Affordable Access

deepdyve-link
Publisher Website

IL-10-producing NK cells exacerbate sublethal Streptococcus pneumoniae infection in the lung.

Authors
  • Clark, Sarah E1
  • Schmidt, Rebecca L2
  • Aguilera, Elizabeth R3
  • Lenz, Laurel L4
  • 1 Department of Otolaryngology, University of Colorado School of Medicine, Aurora, Colorado. Electronic address: [email protected]
  • 2 Department of Biomedical Sciences, National Jewish Health, Denver, Colorado; Department of Biology and Chemistry, Upper Iowa University, Fayette, Iowa.
  • 3 Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado.
  • 4 Department of Biomedical Sciences, National Jewish Health, Denver, Colorado; Department of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, Colorado.
Type
Published Article
Journal
Translational research : the journal of laboratory and clinical medicine
Publication Date
Dec 01, 2020
Volume
226
Pages
70–82
Identifiers
DOI: 10.1016/j.trsl.2020.07.001
PMID: 32634590
Source
Medline
Language
English
License
Unknown

Abstract

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.

Report this publication

Statistics

Seen <100 times