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Lipids regulate peripheral serotonin release via gut CD1d.

Jialie Luo1, Zuojia Chen1, David Castellano2

  • 1Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD, USA.

Immunity
|June 24, 2023
PubMed
Summary
This summary is machine-generated.

Invariant natural killer T (iNKT) cells engage with gut enterochromaffin cells to control serotonin release. This lipid-antigen recognition via CD1d regulates gut motility and homeostasis, influenced by microbial factors.

Keywords:
CD1dKv1.2Pyk2enterochromaffin cellsiNKT cellsserotonin

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Area of Science:

  • Immunology
  • Neuroendocrinology
  • Gastroenterology

Background:

  • Intestinal homeostasis relies on immune and neuroendocrine system crosstalk.
  • Immune cell roles in sensing gut hormones and neurotransmitters are not fully understood.
  • Environmental cues like lipids influence gut signaling.

Purpose of the Study:

  • To investigate how immune cells, specifically invariant natural killer T (iNKT) cells, interact with enterochromaffin (EC) cells.
  • To elucidate the mechanism by which lipid antigens modulate serotonin (5-HT) release from EC cells.
  • To understand the role of microbial lipids in regulating this interaction and its impact on gut homeostasis.

Main Methods:

  • Investigated lipid-mediated interactions between iNKT cells and EC cells.
  • Utilized CD1d-dependent assays to study serotonin release.
  • Analyzed the signaling pathways involving protein tyrosine kinase Pyk2 and potassium conductance.

Main Results:

  • Lipid-engaged iNKT cells promote CD1d-dependent serotonin release from EC cells.
  • Sphingolipids from Bacteroides fragilis inhibit serotonin release.
  • CD1d ligation activates Pyk2, restraining potassium conductance, leading to calcium influx and 5-HT secretion.

Conclusions:

  • Gut chemosensory cells, via iNKT cells and CD1d, selectively perceive lipid antigens.
  • This interaction controls serotonin release, modulating intestinal and systemic homeostasis.
  • Microbial lipids can influence gut-brain communication and homeostasis.