Interleukin-33 contributes to ILC2 activation and early inflammation-associated lung injury during abdominal sepsis.

ABSTRACT: Sepsis is defined as infection with organ dysfunction due to a dysregulated immune response. The lung is one of the most vulnerable organs at the onset of sepsis. Interleukin (IL)-33 can be released by injured epithelial and endothelial cells in the lung and regulate immune activation and infiltration. Therefore, we postulated that IL-33 would contribute to the immune response in the lung during sepsis. Using the cecal ligation and puncture (CLP) sepsis model, we show here that IL-33 contributes significantly to both sepsis-induced inflammation in the lung and systemic inflammatory response in the early phase of sepsis. Despite the higher intra-peritoneal bacterial burden, the absence of IL-33 resulted in less infiltration of neutrophils and monocytes into the lungs in association with low

SUBMITTER: Xu H 

PROVIDER: S-EPMC10116412 | biostudies-literature | 2018 Oct

REPOSITORIES: biostudies-literature