Toxin-Producing Bacteria Staph Aureus Induces Skin Inflammation

MedicalResearch.com Interview with:

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

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.

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Bacterial Nitric Oxide Essential For Staph Bacteria To Colonize Nose

MedicalResearch.com Interview with:

Ferric C. Fang, M.D. Professor of Laboratory Medicine and Microbiology Adjunct Professor of Medicine (Infectious Diseases) Director, Harborview Medical Center Clinical Microbiology Laboratory University of Washington School of Medicine Seattle, WA

Dr. Ferric C. Fang

Ferric C. Fang, M.D.
Professor of Laboratory Medicine and Microbiology
Adjunct Professor of Medicine (Infectious Diseases)
Director, Harborview Medical Center Clinical Microbiology Laboratory
University of Washington School of Medicine
Seattle, WA

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: The Fang lab has a longstanding interest in the interaction between nitric oxide (NO·) and pathogenic bacteria. NO· is an important mediator of the host innate immune response that restricts the growth of invading bacterial pathogens. One of the known actions of NO· is the reversible inhibition of aerobic respiration that results from NO· binding to the heme centers of terminal oxidases.

Like mammalian hosts, many bacteria also possess the ability to enzymatically synthesize NO·. Our latest research investigated the physiological role of the Staphylococcus aureus nitric oxide synthase (saNOS). We discovered that endogenously produced NO· is able to target bacterial terminal oxidases under microaerobic conditions, allowing the bacteria to transition to nitrate respiration when oxygen concentrations are limited and helping to maintain the membrane potential. This process was found to be essential for S. aureus nasal colonization in a mouse model. Thus, a conserved mechanism is involved in both the antimicrobial actions of NO· and the physiological role of NO· in regulating bacterial electron transfer reactions. Interestingly, NO·-heme interactions have been shown to control mitochondrial respiration during hypoxia in mammalian cells.

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