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Review
. 2018 Oct 22:9:2416.
doi: 10.3389/fimmu.2018.02416. eCollection 2018.

Pseudomonas aeruginosa in Chronic Lung Infections: How to Adapt Within the Host?

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Review

Pseudomonas aeruginosa in Chronic Lung Infections: How to Adapt Within the Host?

Emmanuel Faure et al. Front Immunol. .

Abstract

Bacteria that readily adapt to different natural environments, can also exploit this versatility upon infection of the host to persist. Pseudomonas aeruginosa, a ubiquitous Gram-negative bacterium, is harmless to healthy individuals, and yet a formidable opportunistic pathogen in compromised hosts. When pathogenic, P. aeruginosa causes invasive and highly lethal disease in certain compromised hosts. In others, such as individuals with the genetic disease cystic fibrosis, this pathogen causes chronic lung infections which persist for decades. During chronic lung infections, P. aeruginosa adapts to the host environment by evolving toward a state of reduced bacterial invasiveness that favors bacterial persistence without causing overwhelming host injury. Host responses to chronic P. aeruginosa infections are complex and dynamic, ranging from vigorous activation of innate immune responses that are ineffective at eradicating the infecting bacteria, to relative host tolerance and dampened activation of host immunity. This review will examine how P. aeruginosa subverts host defenses and modulates immune and inflammatory responses during chronic infection. This dynamic interplay between host and pathogen is a major determinant in the pathogenesis of chronic P. aeruginosa lung infections.

Keywords: Pseudomonas aeruginosa; bacterial adaptation; chronic lung infection; cystic fibrosis; host evasion; immune evasion.

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References

    1. Cohen TS, Prince A. Cystic fibrosis: a mucosal immunodeficiency syndrome. Nat Med. (2012) 18:509–19. 10.1038/nm.2715 - DOI - PMC - PubMed
    1. Ratner D, Mueller C. Immune responses in cystic fibrosis. Am J Respir Cell Mol Biol. (2012) 46:715–22. 10.1165/rcmb.2011-0399RT - DOI - PubMed
    1. Stoltz DA, Meyerholz DK, Welsh MJ. Origins of cystic fibrosis lung disease. N Engl J Med. (2015) 372:351–62. 10.1056/NEJMra1300109 - DOI - PMC - PubMed
    1. Hayashi F, Smith KD, Ozinsky A, Hawn TR, Yi EC, Goodlett DR, et al. . The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5. Nature (2001) 410:1099–103. 10.1038/35074106 - DOI - PubMed
    1. Zhao Y, Yang J, Shi J, Gong Y-N, Lu Q, Xu H, et al. . The NLRC4 inflammasome receptors for bacterial flagellin and type III secretion apparatus. Nature (2011) 477:596–600. 10.1038/nature10510 - DOI - PubMed

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