Journal
JOURNAL OF INNATE IMMUNITY
Volume 8, Issue 4, Pages 362-373Publisher
KARGER
DOI: 10.1159/000444125
Keywords
CXCR1; Chemokine receptors; Pseudomonas; Neutrophils; Cystic fibrosis; Toll-like receptor 5; Reactive oxygen species
Categories
Funding
- German Research Foundation (DFG, Emmy Noether Programme) [HA 5274/3-1]
- Fritz-Thyssen-Foundation
- CRC685 at Tubingen
- Novartis Foundation
- Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, USA
Ask authors/readers for more resources
Pseudomonas aeruginosa is a key opportunistic pathogen causing disease in cystic fibrosis (CF) and other lung diseases such as chronic obstructive pulmonary disease (COPD). However, the pulmonary host defense mechanisms regulating anti-P. aeruginosa immunity remain incompletely understood. Here we demonstrate, by studying an airway P. aeruginosa infection model, in vivo bioluminescence imaging, neutrophil effector responses and human airway samples, that the chemokine receptor CXCR1 regulates pulmonary host defense against P. aeruginosa. Mechanistically, CXCR1 regulates anti-Pseudomonas neutrophil responses through modulation of reactive oxygen species and interference with Toll-like receptor 5 expression. These studies define CXCR1 as a novel, noncanonical chemokine receptor that regulates pulmonary anti-Pseudomonas host defense with broad implications for CF, COPD and other infectious lung diseases. (C) 2016 S. Karger AG, Basel
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available