Enteric glial adenosine 2B receptor signaling mediates persistent epithelial barrier dysfunction following acute DSS colitis.

ABSTRACT: Intestinal epithelial barrier function is compromised in inflammatory bowel disease and barrier dysfunction contributes to disease progression. Extracellular nucleotides/nucleosides generated in gut inflammation may regulate barrier function through actions on diverse cell types. Enteric glia modulate extracellular purinergic signaling and exert pathophysiological effects on mucosal permeability. These glia may regulate inflammation with paracrine responses, theoretically mediated via adenosine 2B receptor (A_2BR) signaling. As the cell-specific roles of A_2BRs in models of colitis and barrier dysfunction are unclear, we studied glial A_2BRs in acute dextran sodium sulfate (DSS) colitis. We performed and validated conditional ablation of glial A_2BRs

SUBMITTER: Grubisic V 

PROVIDER: S-EPMC9385475 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature