Language
English
Publication Date
11-14-2023
Journal
Nature Communications
DOI
10.1038/s41467-023-42913-z
PMID
37963864
PMCID
PMC10646046
PubMedCentral® Posted Date
11-14-2023
PubMedCentral® Full Text Version
Post-print
Abstract
Toll-like receptor 7 (TLR7) is known for eliciting immunity against single-stranded RNA viruses, and is increased in both human and cigarette smoke (CS)-induced, experimental chronic obstructive pulmonary disease (COPD). Here we show that the severity of CS-induced emphysema and COPD is reduced in TLR7-deficient mice, while inhalation of imiquimod, a TLR7-agonist, induces emphysema without CS exposure. This imiquimod-induced emphysema is reduced in mice deficient in mast cell protease-6, or when wild-type mice are treated with the mast cell stabilizer, cromolyn. Furthermore, therapeutic treatment with anti-TLR7 monoclonal antibody suppresses CS-induced emphysema, experimental COPD and accumulation of pulmonary mast cells in mice. Lastly, TLR7 mRNA is increased in pre-existing datasets from patients with COPD, while TLR7
Keywords
Humans, Animals, Mice, Tryptases, Toll-Like Receptor 7, Imiquimod, Lung, Pulmonary Emphysema, Pulmonary Disease, Chronic Obstructive, Emphysema, Nicotiana, Mice, Inbred C57BL, Chronic inflammation, Toll-like receptors, Chronic obstructive pulmonary disease, Inflammatory diseases
Published Open-Access
yes
Recommended Citation
Liu, Gang; Haw, Tatt Jhong; Starkey, Malcolm R; et al., "TLR7 Promotes Smoke-Induced Experimental Lung Damage Through the Activity of Mast Cell Tryptase" (2023). Faculty and Staff Publications. 1801.
https://digitalcommons.library.tmc.edu/baylor_docs/1801
Included in
Critical Care Commons, Internal Medicine Commons, Medical Sciences Commons, Pulmonology Commons, Sleep Medicine Commons