TLR5 participates in the TLR4 receptor complex and promotes MyD88-dependent signaling in environmental lung injury.

ABSTRACT: Lung disease causes significant morbidity and mortality, and is exacerbated by environmental injury, for example through lipopolysaccharide (LPS) or ozone (O₃). Toll-like receptors (TLRs) orchestrate immune responses to injury by recognizing pathogen- or danger-associated molecular patterns. TLR4, the prototypic receptor for LPS, also mediates inflammation after O₃, triggered by endogenous hyaluronan. Regulation of TLR4 signaling is incompletely understood. TLR5, the flagellin receptor, is expressed in alveolar macrophages, and regulates immune responses to environmental injury. Using in vivo animal models of TLR4-mediated inflammations (LPS, O₃, hyaluronan), we show that TLR5 impacts the in vivo response to LPS, hyaluronan and O₃. We demonstrate

SUBMITTER: Hussain S 

PROVIDER: S-EPMC7032926 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature