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The lungs of cystic fibrosis patients trigger the bacteria Pseudomonas aeruginosa to modify its surface during adaptation to the unusual conditions of the airways in such patients. In the April issue of Nature Immunology, scientists show that the immune cell receptor called TLR4 only recognizes the mutant bacterial surface, which explains why P. aeruginosa is not a problem in healthy lungs, but initiates the chronic lung inflammation commonly seen in cystic fibrosis. Samuel Miller and colleagues from Washington University show that, unlike P. aeruginosa isolated from the lungs of cystic fibrosis patients, environmental or lab-adapted strains of P. aeruginosa are not recognized by TLR4. These highly sensitive receptors signal for intricate inflammatory responses to get underway through their recognition of a surface component of P. aeruginosa called LPS. In patients, the LPS is more highly acetylated compared to the LPS from environmental or lab-adapted bacteria. These data help to explain why those with cystic fibrosis are susceptible to chronic lung inflammation after P. aeruginosa infection -- the mutated form of LPS continually stimulates inflammation, adding to the detrimental environment of the cystic fibrosis lung.
Author contact: Samuel I. Miller
Departments of Medicine and Microbiology
University of Washington
Seattle, USA
Tel: +1 206 616 5107
E-mail millersi@u.washington.edu (C) Nature Immunology press release. Advance Publication available online.
Message posted by: Trevor M. D'Souza
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