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Updated: Feb 8, 2026
08:15
Gastrointestinal Motility Monitor GIMM
Published on: December 1, 2010
31.5K
TRPV4 Channel Signaling in Macrophages Promotes Gastrointestinal Motility via Direct Effects on Smooth Muscle Cells
Jialie Luo1, Aihua Qian2, Landon K Oetjen3
1Center for the Study of Itch, Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Immunity
|July 1, 2018
Summary
Muscularis macrophages (MMs) expressing TRPV4 are crucial for normal gastrointestinal motility. Targeting this pathway may offer new treatments for motility disorders, including chemotherapy-induced hypermotility.
Area of Science:
- Gastroenterology
- Immunology
- Physiology
Background:
- Intestinal macrophages play a key role in gastrointestinal (GI) homeostasis.
- Their specific role in regulating intestinal motility remains incompletely understood.
Purpose of the Study:
- To investigate the role of CX3C chemokine receptor 1-expressing muscularis macrophages (MMs) in regulating GI motility.
- To explore the involvement of the transient receptor potential vanilloid 4 (TRPV4) channel in this process.
Main Methods:
- Selective pharmacologic inhibition of TRPV4.
- Conditional deletion of TRPV4 from macrophages.
- Assessment of intestinal motility.
- Measurement of prostaglandin E2 release.
- Evaluation of colon contraction.
Main Results:
- CX3C chemokine receptor 1-expressing MMs are essential for normal GI motility.
- TRPV4 channels on MMs sense various cues and regulate motility.
- Inhibition or deletion of TRPV4 in macrophages reduced intestinal motility.
- TRPV4 stimulation on MMs triggered prostaglandin E2 release, causing colon contraction independently of the enteric nervous system.
- TRPV4 inhibition reversed chemotherapy-induced GI hypermotility.
Conclusions:
- TRPV4-expressing MMs are critical for maintaining normal GI motility.
- This pathway represents a potential therapeutic target for GI motility disorders.
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