期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 314, 期 2, 页码 L225-L235出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00338.2017
关键词
acidosis; inflammation; Pseudomonas aeruginosa
资金
- National Institutes of Health [P30-RR-032136-01, P30-GM-106394, R21-AI-121820, T32-AI-007363]
- Cystic Fibrosis Foundation Research Development Program Grants [STANTO19R0, STANTO11R0]
Acidic microenvironments commonly occur at sites of inflammation and bacterial infections. In the context of a Pseudomonas aeruginosa infection, we previously demonstrated that acidosis enhances the cellular pro-inflammatory interleukin (IL)-1 beta response in vitro. However, how pH alterations affect in vivo IL-1 beta responses and subsequent IL-1-driven inflammation during infection with P. aeruginosa is unclear. Here, we report that acidosis enhances in vivo IL-1 beta production and downstream IL-1 receptor-dependent responses during infection with P. aeruginosa in models of acute pneumonia and peritonitis. Importantly, we demonstrate that infection with P. aeruginosa within an acidic environment leads to enhanced production of a subset of proinflammatory cytokines, including chemokine (C-X-C) motif ligand 1, IL-6, and chemokine (C-C motif) ligand 2, and increased neutrophil recruitment. Furthermore, with the use of IL-1 receptor type 1-deficient mice, we identify the contribution of the IL-1 signaling pathway to the acidosis-enhanced inflammatory response and pathology. These data provide insights into the potential benefit of pH regulation during bacterial infections to control disease progression and immunopathology.
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