IL-10-producing NK cells exacerbate sublethal Streptococcus pneumoniae infection in the lung.
Department of Otolaryngology, University of Colorado School of Medicine, Aurora, Colorado. Electronic address: [email protected]
Department of Biomedical Sciences, National Jewish Health, Denver, Colorado; Department of Biology and Chemistry, Upper Iowa University, Fayette, Iowa.
Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado.
Department of Biomedical Sciences, National Jewish Health, Denver, Colorado; Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado.
- Published Article
Translational research : the journal of laboratory and clinical medicine
- Publication Date
Dec 01, 2020
Lung inflammation is tightly controlled to balance microbial clearance with the tissue damage that accompanies this response. Bacterial pathogens including Streptococcus pneumoniae (S. pneumoniae) modulate immune regulation by promoting secretion of the anti-inflammatory cytokine IL-10. The important cellular sources of IL-10 that impact protection against different bacterial infections are not well characterized. We find that S. pneumoniaeactivates IL-10 secretion from natural killer (NK) cells in the lung, which restrict host protection in a mouse model of sublethal infection. Direct transfer of wild-type NK cells into the lungs of IL-10-deficient mice drives bacterial expansion, identifying NK cells as a critical source of IL-10 promoting S. pneumoniae infection. The S. pneumoniae virulence protein Spr1875 was found to elicit NK cell IL-10 production in purified cells and in the lungs of live animals. These findings reveal therapeutic targets to combat bacterial-driven immune regulation in the lung. Copyright © 2020 Elsevier Inc. All rights reserved.
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This record was last updated on 02/12/2021 and may not reflect the most current and accurate biomedical/scientific data available from NLM.
The corresponding record at NLM can be accessed at https://www.ncbi.nlm.nih.gov/pubmed/32634590