Open AccessCXCL4 contributes to host defense against acute Pseudomonas aeruginosa lung infection
Author(s) -
Lei Yue,
Zheng Pang,
Hua Li,
Ting Yang,
Lei Guo,
Jie Song,
Junjie Mei,
Xinying Song,
Tian Xie,
Ye Zhang,
Xin He,
TongJun Lin,
Zhongping Xie
Publication year - 2018
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0205521
Subject(s) - pseudomonas aeruginosa , chemokine , microbiology and biotechnology , platelet , immunology , biology , bacterial pneumonia , lung , platelet activation , inflammation , medicine , bacteria , antibiotics , genetics
Platelets have been implicated in pulmonary inflammation following exposure to bacterial stimuli. The mechanisms involved in the platelet-mediated host response to respiratory bacterial infection remain incompletely understood. In this study, we demonstrate that platelet-derived chemokine (C-X-C motif) ligand 4 (CXCL4) plays critical roles in a mouse model of acute bacterial pneumonia using Pseudomonas aeruginosa . Platelets are activated during P . aeruginosa infection, and mice depleted of platelets display markedly increased mortality and impaired bacterial clearance. CXCL4 deficiency impairs bacterial clearance and lung epithelial permeability, which correlate with decreased neutrophil recruitment to BALF. Interestingly, CXCL4 deficiency selectively regulates chemokine production, suggesting that CXCL4 has an impact on other chemokine expression. In addition, CXCL4 deficiency reduces platelet-neutrophil interactions in blood following P . aeruginosa infection. Further studies revealed that platelet-derived CXCL4 contributes to the P . aeruginosa -killing of neutrophils. Altogether, these findings demonstrate that CXCL4 is a vital chemokine that plays critical roles in bacterial clearance during P . aeruginosa infection through recruiting neutrophils to the lungs and intracellular bacterial killing.