Science (New York, N.Y.) · 2025
Type 2 cytokines act on enteric sensory neurons to regulate neuropeptide-driven host defense.
СтатьяНазвание и аннотация: Перевод в очереди
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Barilla Rocky M, Berard Clara, Sun Linyu, Sandhu Sumiti, Zaghouani Sarah, Iyer Krishna S, Altun Gizem, Su Chien-Wen, Deguine Jacques, Singh Vasundhara, Hou Yu, Kusumakar Kanupriya, Rutlin Michael L, Rao Meenakshi, Zaghouani Habib, Shi Hai Ning, Xavier Ramnik J, Kuchroo Vijay K
Аннотация
Enteric nervous system (ENS)-derived neuropeptides modulate immune cell function, yet our understanding of how inflammatory cues directly influence enteric neuron responses during infection is considerably lacking. Here, we characterized a primary enteric sensory neuron (PSN) subset producing the neuropeptides neuromedin U (NMU) and calcitonin gene-related peptide β (CGRPβ) and coexpressing receptors for the type 2 cytokines interleukin-4 (IL-4) and IL-13. Type 2 cytokines amplified NMU and CGRPβ expression in PSNs both in vitro and in vivo, and this was abrogated by PSN-specific Il13ra1 deletion. Deletion of Il13ra1 in PSNs impaired host defense to the gastrointestinal helminth Heligmosomoides polygyrus and blunted muscularis immune responses. Co-administration of NMU23 and CGRPβ rescued helminth clearance deficits and restored anti-helminth immunity, highlighting the essential bidirectional neuroimmune cross-talk regulating intestinal type 2 inflammation.