Abstract
Introduction: Visceral hypersensitivity is a hallmark of irritable bowel syndrome (IBS). A putative involvement of the Transient Receptor Potential Ankyrin-1 (TRPA1) cation channel has been suggested by several animal studies. Main objective of this study is to assess location-specific TRPA1 expression in the colonic mucosa and its correlation with symptom severity in IBS patients.<br /> Methods: Biopsies were obtained from the sigmoid of 30 IBS patients (Rome III; median age 39.0 years, 80 % female) and 23 healthy controls (median age 22.7 years, 43.5 % female). Additional biopsies of the proximal colon were obtained in 24 IBS patients. TRPA1 expression levels were measured in duplicate by quantitative reverse-transcriptase-polymerase-chain-reaction, normalized to GAPDH, and assessed as relative mRNA values using the-2 Delta Ct method. In IBS patients, symptoms were assessed and correlated with TRPA1 expression.<br /> Results: Relative TRPA1 expression in the sigmoid was significantly higher in IBS patients compared to healthy controls (P < 0.001). Within IBS patients TRPA1 expression of sigmoid biopsies was significantly higher compared to proximal colon samples (p < 0.001). No significant correlation was found between TRPA1 expression in sigmoid or proximal colon samples and the symptom severity (abdominal discomfort, abdominal pain and bloating). Conclusion: These findings suggest a potential role for the TRPA1 related pathway as a target for IBS treatment in the future. Since there was no correlation found in the current exploratory study between TRPA1 expression and symptom severity, further research towards the clinical relevance of the increased TRPA1 expression in IBS-patients along with its location-specific expression is warranted.
Original language | English |
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Article number | 103273 |
Number of pages | 7 |
Journal | Autonomic Neuroscience-basic & Clinical |
Volume | 259 |
DOIs | |
Publication status | Published - 1 Jun 2025 |
Keywords
- RECEPTOR POTENTIAL ANKYRIN-1
- MAJOR ROLE
- CAPSAICIN
- INFLAMMATION
- CHANNELS
- COLITIS
- AGONISTS
- NEURONS
- TRPV1
- OIL