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Intestinal epithelial CSE-derived H2S alleviates food allergy via modulating the IL-25/ILC2 axis
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DOI：10.1016/j.apsb.2026.07.046.png)
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Abstract
En 中文
Hydrogen sulfide (H2S), an endogenous gasotransmitter, has garnered increasing attention for its role in modulating immune responses and intestinal barrier function. In this study, diminished jejunal H2S levels and expression of its synthesizing enzyme cystathionine gamma-lyase (CSE) in intestinal epithelium were observed in ovalbumin (OVA)-induced food allergic mice. CSE deficiency aggravated OVA-induced food allergy by activating the IL-25/ILC2 axis and enhancing type 2 immune responses, effects that were reversed by exogenous H2S supplementation. Furthermore, H2S treatment suppressed intestinal epithelial cell-derived IL-25 expression by inhibiting c-Jun. IL-25 neutralization attenuated ILC2-driven type 2 immune responses and alleviated allergic symptoms in OVA-challenged CSE-knockout (Cse–/–) mice. Moreover, ILC2 inhibition diminished type 2 cytokine production and disrupted the IL-25 feedback loop, thereby ameliorating food allergy in Cse–/– mice. These findings highlight that intestinal epithelial CSE-derived H2S alleviates food allergy via the IL-25/ILC2 axis and serves as a potential therapeutic target for allergic diseases.
Keywords:
Food allergy
Hydrogen sulfide
Cystathionine gamma-lyase
Interleukin 25
Type 2 innate lymphoid cells
Ovalbumin
Type 2 immune responses
Tuft cell
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