Abstract:
: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-22BP). 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-22Fc 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 pro-inflammatory role and impairs epithelial barrier function likely through interaction with IL-22.
journal_name
Mucosal Immunoljournal_title
Mucosal immunologyauthors
Abood RN,McHugh KJ,Rich HE,Ortiz MA,Tobin JM,Ramanan K,Robinson KM,Bomberger JM,Kolls JK,Manni ML,Pociask DA,Alcorn JFdoi
10.1038/s41385-019-0188-7subject
Has Abstractpub_date
2019-09-01 00:00:00pages
1231-1243issue
5eissn
1933-0219issn
1935-3456pii
10.1038/s41385-019-0188-7journal_volume
12pub_type
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