PGI2 signaling metabolically reprograms CD4 Th2 cells and represses allergic airway inflammation.

ABSTRACT: Prostaglandin I2 (PGI2) is a lipid mediator known to inhibit T helper 2 (Th2) immune responses and allergic inflammation, but its role in regulating Th2 cell metabolism remains underexplored. Using the Seahorse assay, we evaluated the effects of PGI2 signaling on Th2 cell glycolysis and mitochondrial respiration. Our results show that cicaprost, a stable PGI2 analog, significantly reduced basal, maximal, and spare glycolytic capacities in wild-type Th2 cells, while these effects are absent in Th2 cells lacking the PGI2 IP receptor (IP knockout [KO]). Cicaprost also impaired mitochondrial respiration and adenosine triphosphate production in wild-type Th2 cells, but not in IP KO cells, indicating that PGI2 signaling is essential for these metabolic changes. Further analysis revealed that cic

SUBMITTER: Zhou W 

PROVIDER: S-EPMC12481032 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature