Dental Research / 21.05.2026

[caption id="attachment_73889" align="aligncenter" width="500"]why-regular-dental-care-is-important.jpg Photo by Gustavo Fring[/caption] Historically, medical and dental care have been treated as separate disciplines in the minds of many patients. Most people associate dental visits primarily with cavity prevention, fresh breath, and achieving a bright, confident smile. However, modern clinical research paints a much broader and more complex picture of why oral hygiene is so critical. The human mouth is a literal gateway to the entire body, and neglecting its care can lead to a cascade of medical issues that extend far beyond tooth decay. Establishing a consistent routine with a reliable local dental spot for preventative screenings and professional cleans is actually one of the most effective ways to protect yourself against long-term, chronic systemic inflammation. The mechanism behind this whole-body impact comes down to the immune system's biological response to bacterial overgrowth. When plaque is allowed to accumulate and harden into tartar, it creates a highly protected environment where harmful bacteria thrive along and beneath the gumline. This bacterial invasion triggers an immediate immune response, causing localised inflammation known as gingivitis. If left untreated by a professional, this early-stage condition progresses into periodontitis. Periodontitis is a severe infection that breaks down the soft tissue and bone supporting the teeth, creating pockets where even more bacteria can rapidly multiply.
Dental Research / 19.05.2026

Most people only think about their teeth when something hurts. A twinge. A sensitivity. A filling that feels loose. Then the appointment gets booked, the problem gets fixed, and life moves on until the next issue surfaces. It is understandable. But it misses something important. Your mouth is connected to your heart, your lungs, your blood sugar, and your immune response. Researchers have been mapping these connections for decades, yet most people never hear about them in a routine check-up.

<p>Most people only think about their teeth when something hurts. A twinge. A sensitivity. A filling that feels loose. Then the appointment gets booked, the problem gets fixed, and life moves on until the next issue surfaces.</p> <p>It is understandable. But it misses something important. Your mouth is connected to your heart, your lungs, your blood sugar, and your immune response. Researchers have been mapping these connections for decades, yet most people never hear about them in a routine check-up.</p> <!--more--> <p style="text-align: center;">[ IMAGE 1 ]</p> <hr /> <h2><strong>Your Mouth and Your Heart Have More in Common Than You Think</strong></h2> <p>The mouth hosts hundreds of bacterial species. In a healthy mouth, they coexist without causing problems. When the balance shifts, certain bacteria become destructive. They inflame gum tissue — and that inflammation does not stay put.</p> <p>Studies in cardiovascular medicine have found consistent associations between gum disease and elevated heart disease risk. The mechanism is surprisingly direct: bacteria from infected gum tissue enter the bloodstream and travel to arterial walls. Researchers have actually found oral bacteria inside arterial plaque samples. That shifted the conversation from statistical association to something far more specific.</p> <p>Diabetes adds another layer. People with poorly controlled blood sugar tend to have more severe gum disease, and untreated gum disease appears to make blood sugar harder to regulate in return. It runs both ways. Respiratory health is also gaining attention — bacteria from the mouth have been linked to pneumonia and lung infections, particularly in older adults. In pregnancy, gum disease has been associated with preterm birth and low birth weight, and some health systems now recommend dental check-ups as standard prenatal care.</p> <hr /> <h2><strong>The Inflammation Factor Nobody Talks About</strong></h2> <p>Short-term inflammation is useful — it is the body defending itself. Chronic, low-grade inflammation that drags on for months or years is something else entirely. It sits at the root of heart disease, type 2 diabetes, certain cancers, autoimmune disorders, and cognitive decline.</p> <p>Advanced gum disease is a chronic inflammatory condition. The gums become a persistent source of immune activation, and the chemicals produced — called cytokines — circulate through the body. This is why dental health is no longer just about avoiding cavities. It is about managing one genuine contributor to body-wide inflammation.</p> <p>Gum disease is largely preventable and responds well to treatment. Adults who have drifted away from regular dental care often find that re-establishing it is one of the more impactful decisions they can make. Finding a <a href="https://www.andrewgronowdentalcare.com/locations/brighton/" target="_blank" rel="noopener">dentist in Brighton</a> or a trusted local practice and booking that overdue check-up is a reasonable first step. Not perfection — just professional oversight back in the picture.</p> <p style="text-align: center;">[ IMAGE 2 ]</p> <hr /> <h2><strong>Why Childhood Sets the Trajectory</strong></h2> <p>There is a concept in medicine called the critical window — a period in development when habits and exposures have an outsized effect on long-term outcomes. For oral health, that window opens early. Children who see a dentist regularly from a young age get more than clean teeth. They get comfortable with the environment, and that matters more than most parents realise.</p> <p>Dental anxiety stops many adults from seeking timely care, and a significant amount of that anxiety traces back to early experiences. Primary teeth matter too. They hold space in the jaw for permanent teeth, support speech development, and allow children to eat without pain. When lost too early through decay or infection, they disrupt everything that follows.</p> <p>There is a social dimension as well. Children with visible decay or dental pain often hold back — they avoid smiling, eat less comfortably at school, and stay quiet in class. Getting children into a supportive, child-focused environment early makes a genuine difference. Families who want that specialist approach will find that a dedicated <a href="https://www.dentalsuite.com.au/childrens-dentistry/" target="_blank" rel="noopener">kids dentist Newtown</a> or a similarly focused local practice offers both clinical expertise and the patient manner that makes dental visits manageable rather than dreaded.</p> <p style="text-align: center;">[ IMAGE 3 ]</p> <hr /> <h2><strong>What Good Daily Habits Actually Look Like</strong></h2> <p>Brushing twice a day with fluoride toothpaste is still the foundation. Two minutes is the clinical recommendation — most people do around 45 seconds. A simple phone timer changes this more than any gadget will. Electric toothbrushes consistently outperform manual ones in the research, particularly along the gumline.</p> <p>Flossing clears the contact points between teeth that bristles cannot reach — precisely where decay and gum disease most often begin. If flossing feels awkward, interdental brushes are easier and equally effective. Diet matters more than most people expect, but perhaps not in the way they think. Frequency of sugar exposure is more damaging than total intake. Each sugary encounter triggers an acid attack on enamel lasting around 20 minutes — sipping a soft drink across three hours is far harder on teeth than something sweet eaten once with a meal.</p> <p>Stress is the overlooked factor. It contributes to grinding and clenching during sleep, which wears enamel and can fracture teeth over time. A dentist can spot the signs early and recommend a night guard before real damage accumulates.</p> <hr /> <h2><strong>Why Waiting Almost Always Costs More</strong></h2> <p>A small cavity caught early takes minutes to treat. Left alone, it reaches the nerve — meaning root canal treatment. Left longer still, the tooth may not be salvageable at all. Then comes the extraction, the bone loss, the shifting of adjacent teeth, and eventually the conversation about implants or bridges. At every stage the cost increases. The treatment that costs least and causes least discomfort is always the earliest one.</p> <p>Gum disease follows the same pattern. Early-stage gingivitis reverses with a professional clean and better home care. Advanced periodontitis involves bone loss that cannot be restored, only managed. The only thing separating those two outcomes is usually how long treatment was delayed.</p> <hr /> <h2><strong>Rethinking What Dental Care Is Actually For</strong></h2> <p>Your mouth is not separate from your health — it is part of it. Treating dental care as optional, or as something to deal with only when things go wrong, ignores what the evidence has been building toward for years. For adults, that means a regular check-up rhythm with a practice you trust. For parents, it means introducing dental visits early, keeping them calm and low-key, and not letting your own anxieties pass to your children.</p> <p>The research keeps deepening and the connections between oral health and the rest of the body keep getting clearer. Taking care of your mouth is, increasingly, one of the more straightforward things you can do for your overall health.</p> <hr /> <p style="font-size: 13px; color: #666; background: #f0f0f0; border: 1px solid #d8d8d8; padding: 14px 18px;"><strong>Disclaimer:</strong> The information on MedicalResearch.com is provided for educational purposes only, and is in no way intended to diagnose, cure, or treat any medical or other condition. Some links are sponsored. Products, services and providers are not warranted or endorsed by MedicalResearch.com or Eminent Domains Inc. Always seek the advice of your physician or other qualified health and ask your doctor any questions you may have regarding a medical condition. In addition to all other limitations and disclaimers in this agreement, service provider and its third party providers disclaim any liability or loss in connection with the content provided on this website.</p>

Your Mouth and Your Heart Have More in Common Than You Think

The mouth hosts hundreds of bacterial species. In a healthy mouth, they coexist without causing problems. When the balance shifts, certain bacteria become destructive. They inflame gum tissue — and that inflammation does not stay put. Studies in cardiovascular medicine have found consistent associations between gum disease and elevated heart disease risk. The mechanism is surprisingly direct: bacteria from infected gum tissue enter the bloodstream and travel to arterial walls. Researchers have actually found oral bacteria inside arterial plaque samples. That shifted the conversation from statistical association to something far more specific. Diabetes adds another layer. People with poorly controlled blood sugar tend to have more severe gum disease, and untreated gum disease appears to make blood sugar harder to regulate in return. It runs both ways. Respiratory health is also gaining attention — bacteria from the mouth have been linked to pneumonia and lung infections, particularly in older adults. In pregnancy, gum disease has been associated with preterm birth and low birth weight, and some health systems now recommend dental check-ups as standard prenatal care.
OBGYNE / 11.05.2026

MedicalResearch.com Interview with: [caption id="attachment_73653" align="alignleft" width="150"]Bailey MilnePhD Graduate Student | Epidemiology
Queen's University | Department of Public Health Sciences
Kingston, ON Bailey Milne[/caption] Bailey Milne PhD Graduate Student | Epidemiology Queen's University | Department of Public Health Sciences Kingston, ON A large population-based study using health administrative data from Ontario examines whether endometriosis is associated with an increased risk of congenital anomalies in offspring — with findings that suggest increased monitoring may be warranted for affected pregnancies.
MedicalResearch.com: What is the background for this study? The study was conducted using health administrative data in Ontario. The data was from 2006 to 2021, which resulted in over 1.4 million mother-baby pairs. Endometriosis is an inflammatory condition where the uterine lining grows outside of the uterus, which can result in painful menstruation, intercourse and bowel movements. Roughly 10% of reproductive aged patients have endometriosis, and of those, 30–60% have infertility.
Author Interviews, COVID -19 Coronavirus, Infections, NYU/NYMC / 14.03.2024

MedicalResearch.com Interview with: [caption id="attachment_61434" align="alignleft" width="150"]Mukundan G. Attur, PhDAssociate Professor, Department of Medicine
NYU Grossman School of Medicine Dr. Attur[/caption] Mukundan G. Attur, PhD Associate Professor, Department of Medicine NYU Grossman School of Medicine MedicalResearch.com: What is the background for this study? What are the main findings? Response:  The study investigates the potential protective effects of a genetic variant of IL1RN against inflammation and severe outcomes, particularly in COVID-19. Previous research indicates that carriers of this genetic variant may experience less severe radiographic knee osteoarthritis and decreased inflammation in rheumatoid arthritis patients. Given the emergence of cytokine release syndrome in COVID-19 patients, the researchers sought to understand whether the same genetic variant could offer protection against inflammation and potential death in COVID-19 cases.
Author Interviews, Brain Injury, Brigham & Women's - Harvard, Inflammation / 14.01.2024

MedicalResearch.com Interview with: [caption id="attachment_61250" align="alignleft" width="200"]Samir Mitragotri Ph.D.Hiller Professor of Bioengineering and Hansjorg Wyss Professor of Biologically Inspired Engineering Area Chair, Bioengineering Core Faculty Member, Wyss Institute for Biologically Inspired Engineering Harvard John A. Paulson School Of Engineering And Applied Sciences Prof. Mitragotri[/caption] Samir Mitragotri Ph.D. Hiller Professor of Bioengineering Hansjorg Wyss Professor of Biologically Inspired Engineering Area Chair, Bioengineering Core Faculty Member, Wyss Institute for Biologically Inspired Engineering Harvard John A. Paulson School Of Engineering And Applied Sciences MedicalResearch.com: What is the background for this study? Response: Traumatic brain injury (TBI) has a heavy burden on the world, affecting ~70 million people globally each year. Despite its prevalence, there are no clinically approved treatments beyond symptom management. There is an urgent need to develop effective therapies to alleviate the damage caused by TBI.   MedicalResearch.com:  What do macrophages typically do?  As part of the innate immune system, macrophages migrate to areas of injury to eat pathogens or debris and manage inflammation in response to injury or infection. However, in the majority of cases of TBI, there is no actual infection from a foreign pathogen, leading to excessive inflammation that spreads damage beyond the initial impact.
Author Interviews, Inflammation, Nutrition, Red Meat / 09.11.2023

MedicalResearch.com Interview with: Dr. Alexis C. Wood United States Department of Agriculture (USDA)/ARS Children’s Nutrition Research Center Baylor College of Medicine, TX MedicalResearch.com: What is the background for this study? Response: We know (we think!) that what we eat has a big influence on our health. However, discovering which foods influence our health, and how, is highly challenging. Research investigating this topic should be seen as an on-going process as new results and new study methods emerge, and as the food environment shifts. Red meat is often considered a food that should be minimized in diets designed to support good health. This may seem surprising as red meat is a good source of protein and many other nutrients, but the advice to limit red meat intake is based on several large-scale studies showing associations between red meat consumption and the development of conditions such as type 2 diabetes, and other cardiovascular disease risk related factors. However, newer research, with different designs or approaches, has struggled to conclusively support this association; for example, in studies where the amount of red meat in people’s diet is manipulated, we do not see the expected increases in risk. Other studies have suggested that any associations between red meat intake and chronic disease may reflect confounding effects by adiposity – that is, the increased risk of disease really reflects the increased risk associated with a higher BMI.
Author Interviews, COVID -19 Coronavirus, Inflammation, JAMA, Pediatrics, Race/Ethnic Diversity / 30.11.2020

MedicalResearch.com Interview with: Ellen H. Lee, MD Incident Command System Surveillance and Epidemiology Section New York City Department of Health and Mental Hygiene Long Island City, New York  MedicalResearch.com: What is the background for this study? Response: Published reports of the COVID-19-associated multisystem inflammatory syndrome in children (MIS-C) have described higher proportions of cases among Black and Hispanic children. However, case series are limited by the lack of population-level data, which could help provide context for the racial/ethnic distribution of cases described in these reports. The New York City (NYC) Department of Health and Mental Hygiene required reporting of all possible cases of MIS-C among NYC residents, and for cases meeting MIS-C criteria, applied population denominators to calculate MIS-C incidence rates stratified by race/ethnicity. To help characterize the burden of severe COVID-19 disease in NYC, we also calculated COVID-19 hospitalization rates stratified by race/ethnicity.
Author Interviews, Dental Research, Inflammation / 22.10.2020

MedicalResearch.com Interview with: [caption id="attachment_55718" align="alignleft" width="129"]Prof. Michael Glogauer, D.D.S., Ph.D Faculty of Dentistry, University of Toronto Toronto, ON Canada Dr. Glogauer[/caption] Prof. Michael Glogauer, D.D.S., Ph.D Faculty of Dentistry, University of Toronto Toronto, ON Canada MedicalResearch.com: What is the background for this study? Response: Periodontal disease (PD) affects between 20% and 50% of the global population, with growing evidence supporting its association with other inflammatory diseases, including heart disease, arthritis, and diabetes. Several studies have shown how untreated periodontal disease leads to increased medical care costs for nonoral conditions, including patient hospitalization rates. The interaction of inflammatory diseases with PD suggests a shared, underlying pathology that may be exploited to better manage patients and reduce the economic burden. However, the mechanisms through which these diseases interact are unclear. In periodontal disease, tissue and bone destruction in the mouth is driven by elevated recruitment of white blood cells called polymorphonuclear neutrophils (PMNs), which are activated by the oral disease and recruited from the circulation to sites of inflammation. 
Author Interviews, COVID -19 Coronavirus, Inflammation, Pediatrics / 04.09.2020

MedicalResearch.com Interview with: [caption id="attachment_55330" align="alignleft" width="169"]Alvaro Moreira, MD Assistant Professor, Department of Pediatrics Co-Director Neonatal Nutrition and Bone Institute UT Health San Antonio Dr. Moreira[/caption] Alvaro Moreira, MD Assistant Professor, Department of Pediatrics Co-Director Neonatal Nutrition and Bone Institute UT Health San Antonio MedicalResearch.com: What is the background for this study? Response: Multisystem inflammatory syndrome in children (MIS-C), also known as pediatric inflammatory multisystem syndrome, is a new dangerous childhood disease that is temporally associated with coronavirus disease 2019 (COVID-19). We conducted a systematic review to communicate the typical presentation and outcomes of children diagnosed with this hyperinflammatory condition. 
Author Interviews, COVID -19 Coronavirus, Inflammation / 27.08.2020

MedicalResearch.com Interview with: [caption id="attachment_55211" align="alignleft" width="130"]Sacha Gnjatic, PhD Associate Director of the Human Immune Monitoring Center Associate Professor of Medicine, Oncological Sciences and Pathology Icahn School of Medicine at Mount Sinai Member of the Precision Immunology Institute and The Tisch Cancer Institute Mount Sina Dr. Gnjatic[/caption] Sacha Gnjatic, PhD Associate Director of the Human Immune Monitoring Center Associate Professor of Medicine, Oncological Sciences and Pathology Icahn School of Medicine at Mount Sinai Member of the Precision Immunology Institute and The Tisch Cancer Institute Mount Sinai MedicalResearch.com: What is the background for this study? Would you explain what is meant by cytokine/cytokines? Response: COVID-19 is a disease where inflammation is suspected to play a large role in pathogenicity, possibly more so than the tissue damage created by the virus alone. Cytokines are small soluble proteins that are produced by both immune cells and cells from tissues, and many play a role in signaling such inflammation, to alert of tissue damage or infection. Among these cytokines, interleukin-6 (IL-6), IL-8, IL-1beta, and Tumor Necrosis Factor alpha (TNF-a) have been well established as important markers of pathogenic inflammation. Drugs that counteract these cytokines are routinely use in various inflammatory disease, from rheumatoid arthritis to plaque psoriasis and Crohn’s disease. When the initial wave of SARS-CoV-2 infection hit our hospitals in New York, we therefore wondered whether these cytokines were associated with COVID-19 disease severity and outcome, and hoped that a rapid test to detect them in blood could be useful to make clinical decisions about treatment. We were able to analyze a very large number of patient samples (>1400) in a period of one month, and confirmed our findings in a second smaller cohort.
Author Interviews, COVID -19 Coronavirus / 05.08.2020

MedicalResearch.com Interview with: [caption id="attachment_55027" align="alignleft" width="200"]Pranay Sinha, MD Research Fellow Section of Infectious Diseases Boston University School of Medicine Dr. Sinha[/caption] Pranay Sinha, MD Research Fellow Section of Infectious Diseases Boston University School of Medicine  MedicalResearch.com: What is the background for this study? Response: In the early days of the COVID-19  pandemic there were no evidence-based treatments for severely ill patients infected with this virus. We formed an interdisciplinary group of physicians from departments of adult and pediatric infectious diseases, rheumatology, and pulmonary/critical care as well as clinical pharmacy specialists. Given some promising data from China, we instituted treatment with off-label IL-6 receptor inhibitors (tocilizumab and sarilumab). The rationale was to mitigate the exuberant immune response observed in some patients infected with SARS-CoV-2 (also called cytokine storm or cytokine release syndrome). Quite quickly, we started noticing that giving the drug to our sickest patients wasn’t eliciting dramatic improvement. We reasoned that by the time patients were severely ill and requiring ventilators, the damage to their lungs from the cytokine storm had already taken place. It was like closing the barn door after the horse had already bolted.
Author Interviews, Columbia, Heart Disease, Mediterranean Diet, Women's Heart Health / 13.03.2020

MedicalResearch.com Interview with: [caption id="attachment_53518" align="alignleft" width="177"]Dr. Riddhi Shah, PhD AHA SFRN Postdoctoral Research Fellow Division of Cardiology Columbia University Medical Center New York, New York Dr. Shah[/caption] Dr. Riddhi Shah, PhD AHA SFRN Postdoctoral Research Fellow Division of Cardiology Columbia University Medical Center New York, New York MedicalResearch.com: What is the background for this study? Response: The Mediterranean Diet, characterized by higher intakes of plant foods including plant proteins, monounsaturated fat, fish, and lower consumption of animal products and saturated fat, has long been associated with reduced cardiovascular risk and greater longevity, but the molecular mechanisms underlying these associations have not been fully elucidated. We evaluated associations of an Alternate Mediterranean Diet Score, reflective of adherence to this diet pattern and adapted for US populations, and its components with markers of endothelial inflammation directly measured in endothelial cells harvested from women, including oxidative stress, nuclear factor kappa B (NFκB), and endothelial nitric oxide synthase (eNOS) gene expression.
Author Interviews, Biomarkers, JAMA, Pediatrics / 09.09.2019

MedicalResearch.com Interview with: [caption id="attachment_28740" align="alignleft" width="200"]Elizabeth D. Kantor, PhD MPH Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center NY, NY Dr. Elizabeth D. Kantor[/caption] Elizabeth D. Kantor, PhD MPH Department of Epidemiology and Biostatistics Memorial Sloan Kettering Cancer Center NY, NY MedicalResearch.com: What is the background for this study? Response: There has been recent interest in understanding how exposures in childhood and adolescence relate to later-life health outcomes. Although inflammation is thought to play a role in the etiology of various diseases, little is known about the long-term implications of inflammation in early life. We therefore sought to evaluate how erythrocyte sedimentation rate (ESR), a marker of inflammation, measured among ostensibly healthy men in late adolescence, relates to subsequent cause-specific mortality. We found that men with high inflammation in late adolescence experienced increased mortality due to cancer and cardiovascular disease.
Author Interviews, Gout, NIH, OBGYNE / 04.04.2019

MedicalResearch.com Interview with: [caption id="attachment_48366" align="alignleft" width="160"]Jack A. Yanovski, MD, PhDSenior InvestigatorSection on Growth and Obesity, DIR, NICHDNational Institutes of HealthHatfield Clinical Research CenterBethesda, MD 20892‐1103 Dr. Yanovski[/caption] Jack A. Yanovski, MD, PhD Senior Investigator Section on Growth and Obesity, DIR, NICHD National Institutes of Health Hatfield Clinical Research Center Bethesda, MD 20892‐1103 MedicalResearch.com: What is the background for this study? Response: Studies of both mouse models and people suggest that obesity induced inflammation may promote insulin resistance and progression to diabetes. Others have proposed that suppressing this chronic, low level inflammation may slow the onset of diabetes. Nod-like Receptor Family Pyrin Domain Containing 3 (NLRP3) has recently been shown to play a strong role in promoting the inflammatory state in obesity. Colchicine, traditionally used to suppress or prevent inflammation in gout and other disorders is believed to inhibit formation of the NLRP3 inflammasome. Our group hypothesized that colchicine would improve obesity associated inflammation in adults with metabolic syndrome who had not yet developed type 2 diabetes.
Author Interviews, Dermatology, Lipids / 04.12.2018

MedicalResearch.com Interview with: [caption id="attachment_46353" align="alignleft" width="149"]Wendy Bollag, PhD, FAHA Professor of Physiology VA Research Career Scientist Augusta University, Georgia Dr. Bollag[/caption] Wendy Bollag, PhD, FAHA Professor of Physiology VA Research Career Scientist Augusta University, Georgia MedicalResearch.com: What is the background for this study? Response: We have previously shown that the lipid (fat) phosphatidylglycerol (PG) is able to inhibit rapidly growing keratinocytes (skin cells) and promote their maturation. We also found that PG can suppress skin inflammation. Since the common skin disease psoriasis is characterized by inflammation and excessive growth and abnormal maturation of skin cells, we believed that PG might be useful as a treatment. However, the mechanism of its anti-inflammatory effect was unknown. PG in the lung has been found to inhibit inflammation induced by microbes or their components, which work by activating the innate immune system via binding to proteins called toll-like receptors (TLRs); however, psoriasis is not considered to be an infectious disease. We hypothesized that PG would also inhibit inflammation induced by anti-microbial peptides that activate TLRs. Anti-microbial peptides, produced normally by the skin to protect against infection, are known to be excessively up-regulated in psoriatic skin. 
Author Interviews, Inflammation, Science / 14.06.2018

MedicalResearch.com Interview with: “Basophil” by GreenFlames09 is licensed under CC BY 2.0Jagadeesh BAYRY, DVM, PhD, HDR Scientist CRCN/Associate Professor-INSERM Institut National de la Santé et de la Recherche Médicale (INSERM) Unité 1138 Centre de Recherche des Cordeliers PARIS , FRANCE   MedicalResearch.com: What is the background for this study? What are the main findings? Response: Basophils are rare granulocytes that are important for the protection against helminth parasites. In addition, basophils mediate T helper 2 responses, support B cell differentiation, and thus establish a vital link between innate and adaptive immunity. Although rare in number, basophils are implicated in various pathological conditions due to the fact that they undergo rapid activation in response to a wide range of stimuli they receive. These stimuli induce the release of diverse immune mediators including cytokines and mediators of hypersensitivity reactions histamine and leukotriene. Basophils are well known for their pathogenic role in allergic diseases. Recent data also advocate basophils in the pathogenesis of autoimmune and other inflammatory diseases. Therefore, considering the impact of dysregulated functions of basophils on the immune response in various diseases, we deliberated that it is essential to understand the regulatory mechanisms by which basophils are kept in check. Among immunoregulatory cells, CD4+CD25+FoxP3+ regulatory T cells (Tregs) have been widely studied for their role in immune tolerance and in the maintenance of immune homeostasis. Tregs modulate autoimmune and inflammatory responses by exerting direct suppressive effects on various immune cells including dendritic cells, T cells, macrophages, monocytes, B cells, neutrophils, natural killer cells, and mast cells. In view of emerging reports on the role of basophils in various pathological conditions, we investigated if Tregs are able to control the activation and functions of basophils. In contrast to the central dogma on Tregs as immunosuppressors, we discovered that human basophils are refractory to Treg-mediated suppression. On the contrary, we found that Tregs stimulate resting basophils to induce the expression of activation markers CD69, CD203c, and CD13, and release cytokines IL-4, IL-8, and IL-13. Treg-induced activation of basophils involves IL-3 and STAT5 but was not contact-dependent. These results provide evidence of direct positive effects that human Tregs have on basophil activation and reveal a previously unrecognized feature of this cell subset well known for immunosuppressive functions. 
Author Interviews, Biomarkers, Heart Disease, JAMA, Race/Ethnic Diversity / 04.05.2018

MedicalResearch.com Interview with: [caption id="attachment_41395" align="alignleft" width="200"]Dr. Karl T. Kelsey, MD, MOH Professor of Epidemiology and Pathology and Laboratory Medicine Fellow, Collegium Ramazzini Providence, R.I. 02912 Dr. Kelsey[/caption] Dr. Karl T. Kelsey, MD, MOH Professor of Epidemiology and Pathology and Laboratory Medicine Fellow, Collegium Ramazzini Providence, R.I. 02912 MedicalResearch.com: What is the background for this study? What are the main findings? Response: ​There is a large literature suggesting that the ratio of neutrophils to lymphocytes (the neutrophil to lymphocyte ratio or NLR) in the peripheral blood at the time of diagnosis is robustly predictive ​of outcome in acute cardiovascular disease. We were curious to know if the peripheral blood profile and this ratio was a feature of the disease process, since, to our knowledge, this had not been investigated in a prospective study.  Hence, we used the resources of 2 prospective studies to assess this question, the Jackson Heart Study and the Normative Aging Study.  In both cases, the NLR predicted all cause mortality and, in the Jackson Heart Study, where we had well adjudicated outcomes, the NLR predicted various specific cardiovascular outcomes as well. Interestingly, the outcome was also modified by a well known genetic polymorphism of African origin that results in a relative neutropenia.
Allergies, Author Interviews, Dermatology, Inflammation, Pediatrics / 07.03.2018

MedicalResearch.com Interview with: Nidhi Malhotra PhD Boston Children's Hospital Division of Allergy and Immunology Senior Scientist at Elstar Therapeutics Inc. MedicalResearch.com: What is the background for this study? What are the main findings? Response: Allergies such as Atopic Dermatitis (AD) are rampant in the industrialized nations. Why are we more predisposed to developing hypersensitive reactions to innocuous proteins (allergens) is not well understood. To gain better understanding and to develop better therapies, we need to first delve deeper into how our immune system regulates homeostasis in tissues such as skin. The main cell types that thwart inflammatory reactions are known as regulatory T cells. These cells are generated in thymus and reside in secondary lymphoid tissues but they are also prominent at tissue sites such as in dermal layer of skin. In this study, I focused on understanding how Tregs resident in skin are distinct from the Tregs in secondary lymphoid organs such as lymph nodes (LNs). I uncovered that functioning of Tregs in skin is underpinned by a distinct set of genes. One main gene that I found to be highly expressed in skin Tregs but not in LN Tregs is Rora, which encodes for the transcription factor ROR alpha (RORa). This observation was intriguing as previous studies had elucidated the requirement of RORa in the development of inflammatory type-2 innate lymphoid cells (ILC2s) and it has been considered the antagonizing RORa functioning would curb allergic responses. However, I observed that Tregs require RORa to suppress allergic responses. In particular, RORa regulates the expression of a TNF receptor family member DR3, which binds to the cytokine TL1A. TL1A has a role in enhancing suppressive activity of Tregs while also enhancing type-2 cytokine production from ILC2s. Hence, in the absence of DR3 in Tregs, we believe more TL1A is available to ILC2s resulting in unrestrained allergic responses. 
Author Interviews, Dermatology, Infections, Johns Hopkins / 09.11.2017

MedicalResearch.com Interview with: [caption id="attachment_38127" align="alignleft" width="80"]Lloyd S. Miller, M.D., Ph.D. Vice Chair for Research, Department of Dermatology Associate Professor of Dermatology, Infectious Diseases, Orthopaedic Surgery & Materials Science and Engineering Faculty Member, Cellular and Molecular Medicine (CMM) and Pathobiology Graduate Programs Johns Hopkins Department of Dermatology Baltimore, MD 21231 Dr. Miller[/caption] Lloyd S. Miller, M.D., Ph.D. Vice Chair for Research, Department of Dermatology Associate Professor of Dermatology, Infectious Diseases, Orthopaedic Surgery & Materials Science and Engineering Faculty Member, Cellular and Molecular Medicine (CMM) and Pathobiology Graduate Programs Johns Hopkins Department of Dermatology Baltimore, MD 21231  MedicalResearch.com: What is the background for this study? What are the main findings? Response: Staphylococcus aureus is a common bacterial skin pathogen and its abundance is greatly increased on affected skin of eczema patients, especially during disease flares. However, how S. aureus induces skin inflammation and exacerbates the skin inflammation is incompletely understood. In this study, we found that S. aureus exposure of mouse skin induced skin inflammation through an inflammatory mediator known as IL-36.
Alzheimer's - Dementia, Author Interviews, Johns Hopkins, Memory, Mental Health Research / 04.11.2017

MedicalResearch.com Interview with: Keenan A. Walker, PhD Johns Hopkins University School of Medicine Baltimore, MD MedicalResearch.com: What is the background for this study? What are the main findings? Response: There is quite a bit of evidence linking immune function with dementia. For example, several of the risk genes for Alzheimer’s disease are known to play a key role in immune functioning and the regulation of inflammation. We conducted the current study to determine whether systemic inflammation earlier in life might be a risk factor for neurodegeneration decades later. This long temporal window allows us to get closer to understanding causality. That is, which comes first – systemic inflammation or brain volume loss. Using a large community sample, we found that individuals with higher levels of blood inflammatory markers during midlife tended to have smaller brain volumes in select regions and reduced memory ability as older adults. We found the strongest associations between systemic inflammation and brain volume loss in brain regions most vulnerable Alzheimer’s disease.
Author Interviews, Heart Disease, Inflammation, Nature / 18.04.2017

MedicalResearch.com Interview with: [caption id="attachment_33993" align="alignleft" width="163"]Borja Ibáñez MD Spanish National Centre for Cardiovascular Research Madrid Dr. Ibáñez[/caption] Borja Ibáñez MD Spanish National Centre for Cardiovascular Research Madrid MedicalResearch.com: What is the background for this study? What are the main findings? Response: Acute myocardial infarction (heart attack) is a severe condition responsible for thousands of deaths every year and with important long-term consequences for survivors. Best treatment for acute myocardial infarction is a rapid coronary reperfusion. Upon reperfusion, all inflammatory cells and mediators accumulated in the circulation during the infarction process, enter into the myocardium and causes an extra damage to the heart. Activated neutrophils play a critical role in this damage occurring upon reperfusion. The final size of infarction is the main determinant for mortality and long-term morbidity. The possibility of limiting the extent of infarcted tissue is of paramount importance. Betablockers have been used in patients for more than 4 decades, mainly to treat arrhythmias and high blood pressure. Recently the same group of investigators demonstrated that the very early administration (i.e. during ambulance transfer to the hospital) of the betablocker “metoprolol” was able to reduce the size of infarction in patients. The mechanism by which metoprolol was protective in patients suffering a myocardial infarction was unknown.
Author Interviews, Gastrointestinal Disease, Inflammation, Microbiome, Nature / 19.03.2017

MedicalResearch.com Interview with: Justin E. Wilson, Ph.D On behalf of the authors Research Assistant Professor - Laboratory of Jenny Ting Department of Genetics Lineberger Comprehensive Cancer Center The University of North Carolina at Chapel Hill Chapel Hill, NC 27599 MedicalResearch.com: Could you provide me with some background on this project? Why did you decide to do this research project? What prior work led up to this latest paper? Response: Previous work from our lab and others discovered two major points about NLRP12: a) NLRP12 suppresses inflammation in response to bacterial components b) NLRP12 provides protection against the inflammatory bowel disease colitis and colitis-associated colon cancer (i.e., Nlrp12-defcient mice have greater colon inflammation and inflammation-driven colon cancer). Therefore, we wanted to know if Nlrp12 was regulating inflammation in the colon by responding to the trillions of intestinal microbes collective referred to as the microbiome. Mounting evidence also indicates that the immune system both responds to and influences the composition of the intestinal microbiome during intestinal health and disease, and we hypothesized that NLRP12 could be one of the important immune components during this process. Moreover, we were also interested in this topic because targeting the microbiome to treat inflammatory disorders and other diseases is an attractive method that has many advantages over immune suppression.
Author Interviews, Gastrointestinal Disease, HIV, Inflammation / 15.12.2016

MedicalResearch.com Interview with: Prof. Jamal Tazi Director, Institute for Molecular Genetics CNRS and University of Montpellier and Executive Committee Member ABIVAX MedicalResearch.com: What is the background for this study? Response: Its long been established that people with HIV, even those treated successfully with antiretroviral treatment, exhibit significantly higher levels of chronic inflammation than HIV-negative people. The causes of this inflammation are many – ongoing viral replication, often in the so-called viral reservoirs, leaky gut syndrome, concomitant viral infections (eg CMV, hepatitis etc).
Author Interviews, Biomarkers, JAMA, NIH, Parkinson's / 26.09.2016

MedicalResearch.com Interview with: [caption id="attachment_28339" align="alignleft" width="200"]Yong Cheng, PhD, post-doc fellow Section on Cellular Neurobiology Eunice Kennedy Shriver National Institute of Child Health and Human Development National Institutes of Health Bethesda, Maryland Dr. Yong Cheng[/caption] Yong Cheng, PhD, post-doc fellow Section on Cellular Neurobiology Eunice Kennedy Shriver National Institute of Child Health and Human Development National Institutes of Health Bethesda, Maryland MedicalResearch.com: What is the background for this study? Response: Parkinson’s disease is the second most neurodegenerative disease after Alzheimer’s disease. The symptoms of the disease are typically movement related. However, the nonmotor features in PD are increasingly recognized. Evidence suggests that inflammation may play a role in the development of AD, and a substantial number of studies have demonstrated altered levels of peripheral blood inflammatory cytokines in patients with  Parkinson’s disease, but findings have been inconsistent for individual cytokines and between studies. Therefore, we undertook a systematic review of the scientific literature, using a meta-analysis to quantitatively summarize clinical data on blood cytokine levels in patients with PD, compared with healthy controls.
Author Interviews, Infections, Inflammation / 07.09.2016

MedicalResearch.com Interview with: [caption id="attachment_27723" align="alignleft" width="142"]David Underhill, PhD Professor of Biomedical Sciences Research scientist, F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute Cedars-Sinai Dr. David Underhill[/caption] David Underhill, PhD Professor of Biomedical Sciences Research scientist, F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute Cedars-Sinai Los Angeles, CA MedicalResearch.com: What is the background for this study? Response: “Innate immunity” is the body’s natural resistance to microbial infection and stands in contrast to “adaptive immunity,” which is the body’s learned response to infection (e.g. antibodies and vaccines). In the standard model of innate immunity that has emerged over the last several decades, scientists have come to understand that the human genome encodes many “receptors” that have evolved as sensors for specific common microbial molecules, such as bacterial or viral DNA or components of bacterial or fungal cell walls. The job of these receptors is to survey the environment (skin, blood, etc.) for potentially dangerous microbes and initiate inflammatory responses if they are found. These activities are essential for defense against infection, and people and animals with defects in these sensors or the responses they trigger can be susceptible to infection. My laboratory has been interested for more than a decade in identifying these innate sensors and the microbial targets that they recognize. In this study, we were looking for the sensor that allows white blood cells (e.g. macrophages and dendritic cells) to detect Gram-positive bacterial cell walls and trigger a specific inflammatory response: secretion of the potent inflammatory mediator interleukin-1β (IL-1β).
Alzheimer's - Dementia, Author Interviews, Biomarkers / 01.09.2016

MedicalResearch.com Interview with: [caption id="attachment_27583" align="alignleft" width="125"]Inflammatory Biomarkers May Presage Development of Alzheimer's Prof. Paul Morgan[/caption] Professor B. Paul Morgan Director, Systems Immunity Research Institute Institute of Infection and Immunity School of Medicine Cardiff University MedicalResearch.com: What is the background for this study? Response: Inflammation is a normal response of the body to infection or injury; however, it is well known that inflammation also has a dark side and when it escapes normal controls can cause disease. Some illnesses, like rheumatoid arthritis, have been known for many years to be caused by rogue inflammation and most of the drugs used to treat work by suppressing the inflammation (anti-inflammatories). More recently, it has become clear that inflammation is behind many other diseases that were previously thought of as diseases of ageing caused by wear and tear and lifestyle - these include heart disease and some brain diseases, notably Alzheimer's disease the commonest cause of dementia. Evidence that inflammation is one of the drivers of disease has come from many sources, including some where it was noticed that people on long-term anti-inflammatory drugs for other reasons appeared to be protected from developing Alzheimer's disease. A problem is that Alzheimer's disease, despite the name, is not a single disease but rather a group of conditions with similar symptoms, and inflammation is likely to be a cause in only some of the patients; further, most of the inflammation might be occurring very early in the disease, even before symptoms are obvious. So, there is an urgent need for a simple test or set of tests that can be used in individuals with the very earliest hints of Alzheimer's disease - mild memory loss - that will pick out those who have brain inflammation and are most likely to develop Alzheimer's disease. It might then be possible to treat this select group with anti-inflammatory drugs that will reduce brain inflammation and slow or stop progression of the disease.
Author Interviews, Genetic Research, Pediatrics / 25.11.2015

[caption id="attachment_19630" align="alignleft" width="180"]Grant S Schubert MD, PhD Clinical Fellow, Division of Rheumatology Cincinnati Childrens Hospital Dr. Schulert[/caption] MedicalResearch.com Interview Grant S Schulert MD, PhD Clinical Fellow, Division of Rheumatology Cincinnati Childrens Hospital  Medical Research: What is the background for this study? What are the main findings? Dr. Schulert: Influenza infection causes millions of illnesses annually, but most of those are relatively mild.  In a subset of cases, patients can become critically ill, even if they are relatively young and healthy.  Several previous reports had observed in these critically ill patients features of a hyperinflammatory syndrome known as HLH (hemophagocytic lymphohistiocytosis) or MAS (macrophage activation syndrome).  This hyperinflammation can be triggered by other infections as well as in a subtype of juvenile arthritis, but there is also a familial form occurring in early childhood with known genetic causes.  Our questions with this study were 1) how often are features consistent with HLH/MAS seen in fatal H1N1 influenza infections and 2) do patients with fatal H1N1 infection have genetic mutations associated with HLH/MAS? Our collaborator Paul Harms, MD, and his team at the Michigan Center for Translational Pathology, University of Michigan Medical School identified 16 cases of fatal H1N1 influenza infection.  Based on their clinical features, between 41-88% of these patients could be categorized as having a hyperinflammatory HLH/MAS.  We then used processed tissue samples from the patients for whole exome genetic sequencing, which reads the entire genetic code of every gene in a person. Five patients carried mutations in genes which cause HLH, and several others carried mutations in genes linked to MAS.  This suggests that there may be genetic risk factors for developing fatal hyperinflammatory syndromes in H1N1 infection.
Author Interviews, Inflammation, Lipids, University of Pennsylvania / 04.08.2015

Carsten C. Skarke MD Research Assistant Professor of Medicine McNeil Fellow in Translational Medicine Institute for Translational Medicine and Therapeutics Perelman School of Medicine University of PennsylvaniaMedicalResearch.com Interview with: Carsten C. Skarke MD Research Assistant Professor of Medicine McNeil Fellow in Translational Medicine Institute for Translational Medicine and Therapeutics Perelman School of Medicine University of Pennsylvania Medical Research: What is the background for this study? What are the main findings? Dr. Skarke: A growing body of publications suggests anti-inflammatory actions of fish oils. These health benefits are proposed to emerge from lipids called specialized pro-resolving mediators, (SPMs), which can be formed from omega-3 polyunsaturated fatty acids found in fish. A limitation to date, though, in this field is that there is little evidence of their formation in humans. And the cases where presence of these lipids is reported in humans, less rigorous analytical approaches, such as enzyme immunoassay (EIA), radioimmunoassay (RIA) or mass spectrometry without internal authentic standards, have been used. Thus, the specific aim for our study was to use state-of-the-art mass spectrometry to identify and quantify these specialized pro-resolving mediators. Several aspects of our study design set us apart from what was done in previous studies.
  • First, we biased our ability to detect SPMs formed in healthy volunteers by giving fish oil in high doses which had been previously shown to influence blood pressure and platelet aggregation under placebo-controlled conditions.
  • Second, we also looked at lower doses of fish oil, those more commonly consumed by the general public, for the formation of SPMs during an acute inflammatory response and its resolution.
  • Third, we relied in our measurements of SPMs on authentic internal standards. These deuterated lipids, d4-resolvin E1 for example, facilitate distinct identification of the naturally formed lipid.
  • And fourth, we achieved very low limit of detection levels, below 10 pg/ml for resolvin E1, for example.
The surprising finding of our studies is that we failed to detect a consistent signal of SPM formation in urine or plasma of healthy volunteers who had taken fish oil. Even more surprising was that we found no alteration in the formation of SPMs during the resolution of inflammation. These results let us question the relevance of endogenous specialized pro-resolving mediators to the putative anti-inflammatory effects of fish oils in humans.
Author Interviews, Brain Injury, Inflammation / 21.01.2015

Alan I Faden, M.D. David S. Brown Professor in Trauma Professor, Departments of Anesthesiology, Anatomy & Neurobiology, Neurosurgery, and Neurology Director, Center for Shock, Trauma & Anesthesiology Research (STAR) University of Maryland School of MedicineMedicalResearch.com Interview with: Alan I Faden, M.D. David S. Brown Professor in Trauma Professor, Departments of Anesthesiology, Anatomy & Neurobiology, Neurosurgery, and Neurology Director, Center for Shock, Trauma & Anesthesiology Research (STAR) University of Maryland School of Medicine Medical Research: What is the background for this study? What are the main findings? Dr. Faden: Accumulating clinical and pre-clinical research data indicate that traumatic brain injury (TBI) can lead to chronic progressive neurodegeneration. In this regard, most attention has focused on the connections between TBI and with Alzheimer disease (AD) or Chronic Traumatic Encephalopathy (CTE). However, recent epidemiological studies raise questions about the association between TBI and AD, and CTE is likely a less common end-stage result resulting from complex pathobiological changes. In contrast, both older and newer studies underscore that traumatic brain injury can cause chronic neuroinflammation that leads to chronic neurodegeneration. In contrast to AD and CTE, the latter condition appears to be potentially treatable, even long after injury. Our paper critically assesses the mechanisms and treatment of chronic post traumatic neurodegeneration.