Abstract
Abstract
Background
Functional Gastrointestinal disorders (FGIDs) are highly prevalent among adolescents. Increased intestinal permeability plays a potential role in the pathogenesis of FGIDs. Claudin-3 (CLDN3) may serve as an indicator of gut barrier integrity. We aimed to assess serum level of CLDN3 as a noninvasive biomarker of intestinal permeability in adolescents with FGIDs, and its relation with inflammatory markers.
Methods
This study included 70 adolescents with FGIDs and 65 healthy controls. Serum levels of CLDN3 and inflammatory markers; C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα), and haptoglobin, were measured using enzyme-linked immunosorbent assay.
Results
Serum levels of CLDN3 and inflammatory markers; CRP, Il-6, TNFα and haptoglobin, were significantly higher in cases compared to controls (
p
= 0.02, 0.039, 0.04, 0.021 and 0.001, respectively). We detected significant positive correlations between serum level of CLDN3 and that of CRP, IL-6 and haptoglobin in cases.
Conclusion
Our results revealed significant elevations in serum levels of CLDN3 and inflammatory markers in adolescents with FGIDs. Significant positive correlations were detected between levels of CLDN3 and that of CRP, IL-6 and haptoglobin, suggesting an association between intestinal barrier dysfunction and low-grade systemic inflammation. Thus, CLDN3 represents a potential noninvasive biomarker of intestinal permeability in FGIDs.
Impact
This research investigated the potential role of Claudin-3 (CLDN3) as a noninvasive biomarker of intestinal permeability in adolescents with Functional Gastrointestinal Disorders (FGIDs), and its relation to the inflammatory status of these patients.
To the best of our knowledge, this is the first study to assess serum CLDN3 as a noninvasive biomarker of intestinal permeability in FGIDs; previous researches have assessed intestinal barrier disruption in FGIDs based on intestinal biopsies.
Our findings suggest that impaired intestinal barrier function may promote development of FGIDs by inducing inflammation. Thus, restoration of intestinal barrier integrity may represent a potential therapeutic target for FGIDs.