Neuronal-Activated ILC2s Promote IL-17A Production in Lung γδ T Cells During Sepsis.

ABSTRACT:

Background

Studies have revealed important roles for IL-17A in the development of acute lung injury (ALI) following sepsis. However, the mechanism underlying the regulation of lung IL-17A remains to be fully addressed. Recent studies suggested the effect of neuromedin U (NMU) on immune cell activation and the role of group 2 innate lymphoid cells (ILC2s) in the modulation of IL-17A production. We aimed to gain in-depth insight into the mechanism underlying sepsis-induced lung IL-17A production, particularly, the role of NMU in mediating neuronal regulation of ILC2s and IL-17A-producing γδ T cells activation in sepsis.

Methods

Wild type mice were subjected to cecal ligation and puncture (CLP) to induce sepsis with or without intraperitoneal injection of NMU. The levels of ILC

SUBMITTER: Chen W 

PROVIDER: S-EPMC8119647 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature