NF-kappaB dependent inflammatory response modulates by Toll-like receptor in sepsis

 

"Research Article"

American Journal of BioMedicine  Volume 3, Issue 3, pages 134-140, March 2015


Delbert N.Thota; Anna Oddis; Gurpreet Banerjee; Hiroshi Caudell, Roschelle Ohura

Abstract

Toll-like receptor 4 (TLR4), as a membrane surface receptor for bacterial, fungal, viral and certain endogenous substances, has been described to contribute to the development of sepsis. Wild-type mice and HJN mice were treated with intraperitoneal lipopolysaccharide (LPS) then serum and tissue from myocardium, lung and kidney analysis proinflammatory response using double immunofluorescence, histopathology stain, western blott, and ELISA. We repeated this experiment in chimeric mice lacking NF-kappaB expression. From these experimental data, the TLR4 is overactivated in sepsis and induce proinflammatory response through upregulation of NF-kappaB expression. Further experimental research is needed, especially of the study of biochemical markers of the injury process to establish the role of TLR4 in sepsis.

Keywords: Sepsis; TLR4; lipopolysaccharide; NF-kappaB


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