Toll-like receptor (TLR)-based networks regulate neutrophilic inflammation in respiratory disease.
The neutrophil is a crucial early defence against microbial infection, but neutrophilic inflammation can result in devastating acute and chronic inflammatory diseases. In the lungs, the neutrophil is a principal part of the pathology of the acute respiratory distress syndrome, and its activation may also be of substantial importance in chronic obstructive pulmonary disease and some forms of asthma. Induction of neutrophil recruitment in response to microbial attack requires activation of TLR (Toll-like receptor)-based signalling pathways and the concerted actions of multiple cell types, including sentinel cells such as monocytes and macrophages acting together with tissue cell types such as the epithelium or smooth-muscle cell. The present review describes some of these networks and the resulting potential for their targeting in respiratory disease.
Sabroe
I
I
Academic Unit of Respiratory Medicine, Section of Infection, Inflammation and Immunity, School of Medicine and Biomedical Sciences, Royal Hallamshire Hospital, University of Sheffield, Sheffield S10 2JF, U.K. i.sabroe@sheffield.ac.uk
Whyte
M K B
MK
D000818:Animals; D006801:Humans; D007249:Inflammation; D020556:Neutrophil Infiltration / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D012141:Respiratory Tract Infections / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology; D051193:Toll-Like Receptors / Q000276:immunology*
D051193:Toll-Like Receptors