MedicalResearch.com Interview with:
[caption id="attachment_48391" align="alignleft" width="125"]
Dr. Lucas[/caption]
Rudolf Lucas, PhD
Professor Pharmacology and Toxicology
Vascular Biology Center, Division of Pulmonary Medicine
[caption id="attachment_48392" align="alignleft" width="129"] Dr. Madaio[/caption]
Michael P. Madaio, MD
Sydenstricker Professor and Chairman
Department of Medicine
Medical College of Georgia
Augusta University
Augusta, Georgia 30912, USA.
MedicalResearch.com: What is the background for this study?
Response: The pro-inflammatory cytokine tumor necrosis factor (TNF) is a crucial mediator of glomerulonephritis, but the cytokine is also important in defense to bacterial infections. As such, chronically inhibiting TNF, using soluble TNF receptor constructs or neutralizing anti-TNF antibodies can promote infection.
In this study, we wanted to develop a novel therapeutic strategy to specifically inhibiting deleterious TNF signaling, while preserving the beneficial anti-bacterial actions of the cytokine.
Dr. Lucas[/caption]
Rudolf Lucas, PhD
Professor Pharmacology and Toxicology
Vascular Biology Center, Division of Pulmonary Medicine
[caption id="attachment_48392" align="alignleft" width="129"]
Dr. Madaio[/caption]
Michael P. Madaio, MD
Sydenstricker Professor and Chairman
Department of Medicine
Medical College of Georgia
Augusta University
Augusta, Georgia 30912, USA.
MedicalResearch.com: What is the background for this study?
Response: The pro-inflammatory cytokine tumor necrosis factor (TNF) is a crucial mediator of glomerulonephritis, but the cytokine is also important in defense to bacterial infections. As such, chronically inhibiting TNF, using soluble TNF receptor constructs or neutralizing anti-TNF antibodies can promote infection.
In this study, we wanted to develop a novel therapeutic strategy to specifically inhibiting deleterious TNF signaling, while preserving the beneficial anti-bacterial actions of the cytokine.