Toll-like receptors in the host defense against Pseudomonas aeruginosa respiratory infection and cystic fibrosis

SM McIsaac, AW Stadnyk, TJ Lin - Journal of leukocyte biology, 2012 - academic.oup.com
SM McIsaac, AW Stadnyk, TJ Lin
Journal of leukocyte biology, 2012academic.oup.com
Review of innate cell TLR activation by Pseudomonas aeruginosa to explain lung
inflammation during cystic fibrosis, and the prospects of preventing infection. TLRs function
in innate immunity by detecting conserved structures present in bacteria, viruses, and fungi.
Although TLRs do not necessarily distinguish pathogenic organisms from commensals, in
the context of compromised innate immunity and combined with pathogensˈ effector
molecules, TLRs drive the host response to the organism. This review will discuss the …
Abstract
Review of innate cell TLR activation by Pseudomonas aeruginosa to explain lung inflammation during cystic fibrosis, and the prospects of preventing infection.
TLRs function in innate immunity by detecting conserved structures present in bacteria, viruses, and fungi. Although TLRs do not necessarily distinguish pathogenic organisms from commensals, in the context of compromised innate immunity and combined with pathogensˈ effector molecules, TLRs drive the host response to the organism. This review will discuss the evidence and role(s) of TLRs in the response to the opportunistic bacterial pathogen, Pseudomonas aeruginosa, as it relates to respiratory infection and CF, in which innate immune mechanisms are indeed compromised. Outer membrane lipoproteins, LPS, flagellin, and nucleic acids all serve as ligands for TLR2, -4, -5, and -9, respectively. These TLRs and their respective downstream effector molecules have proven critical to the host response to P. aeruginosa, although the protective effects of TLRs may be impaired and in some cases, enhanced in the CF patient, contributing to the particular susceptibility of individuals with this disease to P. aeruginosa infection.
Oxford University Press