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

Journal of Leukocyte Biology

Andrew W. Stadnyk, , and¹  Tong-Jun Lin, ¹  Shayla M. McIsaac¹ 

[1] Departments of Microbiology and Immunology and  Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada

关键词: MyD88;    TRIF;    MAP kinases;   

DOI  :  10.1189/jlb.0811410

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

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 pathogens' 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.

【 授权许可】

Unknown