Abstract

The lung environment is designed to prevent innate responses to harmless commensal microorganisms and environmental antigens. Features of an intact respiratory epithelium are critical to this process. A damaged or altered lung epithelial surface will therefore remove or alter the suppressive signals delivered to local innate immune cells, and inflammation ensues. Timely resolution of inflammation is important to prevent bystander tissue damage. However, if resolving pathways themselves are prolonged or repeated, they too can cause undesirable consequences, including bacterial superinfections, which we discuss here.

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