Targeting the IL-22/IL-22BP axis enhances tight junctions and reduces inflammation during influenza infection.

ABSTRACT: The seasonal burden of influenza coupled with the pandemic outbreaks of more pathogenic strains underscore a critical need to understand the pathophysiology of influenza injury in the lung. Interleukin-22 (IL-22) is a promising cytokine that is critical in protecting the lung during infection. This cytokine is strongly regulated by the soluble receptor IL-22-binding protein (IL-22BP), which is constitutively expressed in the lungs where it inhibits IL-22 activity. The IL-22/IL-22BP axis is thought to prevent chronic exposure of epithelial cells to IL-22. However, the importance of this axis is not understood during an infection such as influenza. Here we demonstrate through the use of IL-22BP-knockout mice (il-22ra2^-/-) that a pro-IL-22 environment reduces pulmonary inflammation

SUBMITTER: Hebert KD 

PROVIDER: S-EPMC6917921 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature