期刊
MUCOSAL IMMUNOLOGY
卷 12, 期 5, 页码 1231-1243出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41385-019-0188-7
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类别
资金
- NIH NHLBI [R01HL107380]
- Pennsylvania Department of Health
- NIDDK [P30DK072506]
- [T32HL129949]
Secondary bacterial pneumonia is a significant complication of severe influenza infection and Staphylococcus aureus and Streptococcus pneumoniae are the primary pathogens of interest. IL-22 promotes S. aureus and S. pneumoniae host defense in the lung through epithelial integrity and induction of antimicrobial peptides and is inhibited by the soluble decoy receptor IL-22-binding protein (IL-228P). Little is known about the effect of the IL-22/IL-22BP regulatory pathway on lung infection, and it has not been studied in the setting of super-infection. We exposed wild-type and IL-22BP(-/-) mice to influenza A/PR/8/34 for 6 days prior to infection with S. aureus (USA300) S. pneumoniae. Super-infected IL-22BP(-/-) mice had decreased bacterial burden and improved survival compared to controls. IL-22BP(-/-) mice exhibited decreased inflammation, increased lipocalin 2 expression, and deletion of IL-22BP was associated with preserved epithelial barrier function with evidence of improved tight junction stability. Human bronchial epithelial cells treated with IL-22BP(-/-) showed evidence of improved tight junctions compared to untreated cells. This study revealed that IL-22BP(-/-) mice are protected during influenza, bacterial super-infection, suggesting that IL-22BP has a proinflammatory role and impairs epithelial barrier function likely through interaction with IL-22
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