期刊
JOURNAL OF INFECTIOUS DISEASES
卷 207, 期 10, 页码 1544-1555出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jit059
关键词
infection; biofilm; Pseudomonas aeruginosa; p38 MAPK; neutrophils; Cystic Fibrosis; cytokines
资金
- Natural Sciences and Engineering Research Council of Canada
- Cystic Fibrosis Canada
- Les Fonds de la Recherche en Sante du Quebec (FRSQ)
- CIHR Strategic Training Initiative in Chemical Biology
- FRSQ
- Canadian Institute of Health Research (CIHR)
- Cystic Fibrosis Canada studentship
- CIHR
Biofilm microcolonies of Pseudomonas aeruginosa chronically infect the airways of patients with cystic fibrosis and fuel ongoing destructive inflammation, yet the impact of the switch from planktonic to biofilm growth on host responses is poorly understood. We report that in airway epithelial cells a threshold of p38 alpha mitogen-activated protein kinase (MAPK) activation was required to trigger neutrophil recruitment, which is influenced by extrinsic and intrinsic factors. Planktonic P. aeruginosa diffusible material (PsaDM) induced stronger p38 alpha MAPK activation as compared to biofilm PsaDM. Biofilm PsaDM activated p38 alpha MAPK in a Toll-like receptor-independent fashion via the lasI/lasR quorum-sensing system, but this activation was insufficient to recruit neutrophils. However, in airway epithelial cells from patients with cystic fibrosis with hypersensitivity to injurious stimuli, biofilm PsaDM activated p38 alpha MAPK strongly enough to recruit neutrophils, which can contribute to lung injury.
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