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Neuroepithelial VIP-VIPR1 interactions differentially control enteric type 1 and type 2 immunity.

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Enteric neurons and gut epithelial cells coordinate immunity via VIP-VIPR1 signaling. This neuroepithelial interaction distinctly controls type 1 and type 2 immune responses in the intestine.

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Area of Science:

  • Neuroimmunology
  • Gastroenterology
  • Innate Immunity

Background:

  • The nervous and immune systems interact to maintain mucosal barrier integrity.
  • The role of enteric neurons in coordinating gut immunity via neuroepithelial interactions is not fully understood.

Purpose of the Study:

  • To identify neuroepithelial interactions that regulate intestinal type 1 and type 2 immunity.
  • To elucidate the function of vasoactive intestinal peptide receptor 1 (VIPR1) in gut epithelial cells and its interaction with enteric neurons.

Main Methods:

  • Chemogenetic modulation of enteric VIPergic neurons.
  • Epithelial-specific gene deletion of Vipr1.
  • Analysis of immune cell populations and cytokine profiles.
  • Assessment of host susceptibility to bacterial and parasitic infections.

Main Results:

  • Gut epithelial cells express VIPR1, and its modulation affects epithelial-derived cytokines.
  • Epithelial-intrinsic Vipr1 deletion impairs type 1 immunity (reduced alarmins, intraepithelial lymphocytes).
  • Epithelial Vipr1 deficiency enhances type 2 immunity (increased alarmins, tuft cells, ILC2s).
  • Disruption of neuroepithelial VIP-VIPR1 signaling increases susceptibility to bacterial infection but enhances resistance to parasite infection.

Conclusions:

  • Neuroepithelial interactions involving VIP and VIPR1 play a critical role in differentially regulating intestinal type 1 and type 2 immunity.
  • This axis represents a novel multi-tissue mechanism for programming gut immune responses.
  • Understanding these interactions is crucial for developing therapeutic strategies against enteric infections.