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TRIF is essential for the clearance of Pseudomonas aeruginosa from the mouse lung
Author(s) -
Power Melanie Rose,
Yamamoto Masahiro,
Akira Shizuo,
Lin TongJun
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a651
Subject(s) - trif , pseudomonas aeruginosa , lung , microbiology and biotechnology , immunology , signal transduction , lung infection , toll like receptor , biology , medicine , innate immune system , immune system , bacteria , genetics
Toll‐IL‐1 receptor domain‐containing adapter‐inducing IFN‐β (TRIF) and MyD88 are adaptor molecules that mediate two distinct Toll‐like receptor (TLR) signaling pathways. The MyD88 pathway is critical for the defense against a number of bacteria. Using a MyD88‐deficient animal model, we showed an important role of the MyD88 pathway in the host defense against Pseudomonas aeruginosa lung infection. Roles of TRIF in the host defense have largely been associated with virus infections. Here we investigated a role of TRIF in P. aeruginosa lung infection. TRIF deficient mice showed severe impairment in the clearance of P. aeruginosa from the lung when compared with wild type mice. A TRIF deficiency impairs production of a selective profile of cytokines and chemokines following P. aeruginosa lung infection. Interestingly, TRIF deficient and TRIF‐MyD88 double deficient mice showed similar levels of impairment in the clearance of P. aeruginosa from the lung and cytokine production, suggesting a major role of TRIF in P. aeruginosa lung infection. This study demonstrates for the first time that TRIF pathway is involved in the host defense against P. aeruginosa lung infection. Thus, the full development of host responses to P. aeruginosa lung infection requires both TRIF‐ and MyD88‐dependent mechanisms. Research funded by grants from CIHR, CCFF amd the IWK Health Centre