Abstract
Pulmonary infection is a leading cause of hospitalization in world. Lung damage due to infection and host mediated pathology can have life threatening consequences. Factors that limit lung injury and/or promote epithelial barrier function and repair are highly desirable as immunomodulatory therapeutics. Over the last decade, interleukin−22 has been shown to have pulmonary epithelial protective functions at the mucosal immune interface with bacterial and viral pathogens. This article summarizes recent findings in this area and provides perspective regarding the role of IL-22 in mucosal host defense.
Highlights
Protective immune mechanisms of lung injury during infection are an important area of research that could provide new immunomodulatory therapeutic options
While data exist regarding the effects of IL-22 on epithelial cells in vitro, there remains much to be discovered
It will be important to assess the effects of IL-22 on epithelial cells in inflammatory settings, perhaps in combination with pathogen associated molecular patterns (PAMPs) or toxins
Summary
Protective immune mechanisms of lung injury during infection are an important area of research that could provide new immunomodulatory therapeutic options. Deletion or antibody neutralization of IL22 resulted in increased lung bacterial burden and dissemination compared with controls during Staphylococcus aureus infection [11] These data are consistent with a barrier protective role for IL-22 in the lung. In the K. pneumoniae model, IFNλR–/– mice exhibited better bacterial control and improved epithelial barrier function [14] These IFNλR–/–mice had acute elevations in IL-22 production suggesting that IFNλ negatively regulates IL-22 in the lung. IL22 therapy increased epithelial barrier function and decreased lung leak In support of these findings, deletion of IL22BP in mice improved outcomes of influenza super-infection with both S. aureus and S. pneumoniae [30]. IL-22 treatment of air liquid interface cultures of human bronchial epithelial cells resulted in preserved tight junction function following injury with S. aureus These data demonstrate and important role for IL-22/IL-22BP in the context of polymicrobial infection. Data is needed to assess the potential for targeting the IL-22 pathway in this context
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