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<p>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-F<sup>hi</sup> neutrophils capable of enhancing Th17 cell differentiation and aggravating asthma symptoms in mouse models. Our results thus implicate GPR43 as a critical regulator of eosinophils, and describe eosinophil-mediated modulation of neutrophil differentiation and function.</p>

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GPR43 in eosinophils suppresses the emergence of pathogenic Siglec-Fhi neutrophils in allergic airway inflammation in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月26日

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  • Jihyun Yu,
  • Seongryong Kim,
  • Hyun-Sup Song,
  • Jieun Kim,
  • Woojung Shin,
  • Jong-Eun Park,
  • Ikuo Kimura,
  • Hye-Young Kim,
  • You-Me Kim

摘要

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 of enhancing Th17 cell differentiation and aggravating asthma symptoms in mouse models. Our results thus implicate GPR43 as a critical regulator of eosinophils, and describe eosinophil-mediated modulation of neutrophil differentiation and function.