ACTIVATION OF THE ARYL HYDROCARBON RECEPTOR REDUCES VISCERAL HYPERSENSITIVITY IN A MOUSE MODEL OF COLITIS IN REMISSION

Oral indole-3-pyruvic acid (IPyA) activates nociceptor aryl hydrocarbon receptor (AhR) and reduces visceral hypersensitivity in male and female post-colitis mice.

• Why it matters: About 50% of inflammatory bowel disease (IBD) patients have chronic abdominal pain even when inflammation is in remission, and reduced indole-derived AhR ligands may contribute to heightened nociception.
• What they did: In a post-colitis mouse model, AhR activation with natural and synthetic agonists reduced visceral hypersensitivity, while AhR inhibition blocked indole-driven antinociception; IPyA increased Kir2.2 transcription in TRPV1+ neurons.
• The result: AhR activation by IPyA markedly reduced dorsal horn neuronal activation and suggests AhR-targeted therapy could treat abdominal pain in IBD patients in remission.

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