GPR43 in eosinophils suppresses the emergence of pathogenic Siglec-F<sup>hi</sup> neutrophils in allergic airway inflammation in mice.
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ABSTRACT: Eosinophils are major effector cells in type 2 immune responses, contributing to host defense and allergic diseases. They also contribute to maintaining tissue homeostasis by regulating various immune cell types, including neutrophils. Here we show that eosinophils directly associate with neutrophils in the lungs of asthma-induced mice. Eosinophil-specific deficiency of the short-chain fatty acid receptor, GPR43, results in hyperactivation of eosinophils and increases the expression of neutrophil chemoattractants and PECAM-1, thereby enhancing the interaction between eosinophils and neutrophils. This interaction exposes neutrophils to eosinophil-derived IL-4 and GM-CSF, which induce the conversion of conventional neutrophils into more pathogenic, Siglec-Fhi neutrophils capable o
SUBMITTER: Yu J
PROVIDER: S-EPMC12657986 | biostudies-literature | 2025 Nov
REPOSITORIES: biostudies-literature
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