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Cysteinyl leukotrienes and acetylcholine are biliary tuft cell cotransmitters
Maryam Keshavarz1,2, Schayan Faraj Tabrizi1,2, Anna-Lena Ruppert3
1Institute of Anatomy and Cell Biology, German Center for Lung Research, Justus Liebig University Giessen, Giessen, Germany.
Science Immunology
|March 4, 2022
Summary
Intestinal bacteria metabolite propionate activates gallbladder tuft cells. This triggers mucin release and gallbladder contraction, representing a dual innate defense mechanism against the gut microbiome.
Area of Science:
- Gastroenterology
- Cell Biology
- Microbiome Research
Background:
- The gallbladder epithelium is exposed to the intestinal microbiome, necessitating antimicrobial defenses.
- Cholangiocytes produce mucins, but the role of biliary tuft cells in gallbladder function remains unclear.
Purpose of the Study:
- To investigate the function of biliary tuft cells in sensing microbial metabolites and mediating gallbladder responses.
Main Methods:
- Activation of tuft cells by propionate via specific receptors (FFAR2, TRPM5).
- Analysis of downstream signaling pathways and mediator release (acetylcholine, cysteinyl leukotrienes).
- Assessment of paracrine effects on cholangiocytes and gallbladder smooth muscle.
Main Results:
- Propionate activates tuft cells, leading to acetylcholine and cysteinyl leukotriene corelease.
- Acetylcholine stimulates mucin release from cholangiocytes via M3 receptors.
- Cysteinyl leukotrienes induce gallbladder contraction via CysLTR1 receptors.
Conclusions:
- Gallbladder tuft cells act as sensors for the microbial metabolite propionate.
- Tuft cells initiate a dual innate defense: mucin secretion and gallbladder emptying.
- This mechanism represents a coordinated response to intestinal microbiome exposure.
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