Correlation Between Adhesion Molecules (ICAM-1 & E-Selectin) and Diagnostic Antibodies (TTG & AGA) in Celiac Disease

Background: Celiac disease (CD) is a chronic autoimmune disorder triggered by gluten ingestion in genetically susceptible individuals, characterized by intestinal inflammation, villous atrophy, and the production of specific autoantibodies, including anti-tissue transglutaminase (TTG) and anti-deamidated gliadin peptides (AGA). Endothelial adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and E-selectin, play a pivotal role in immune cell recruitment and inflammation. Objective: This study aimed to evaluate the correlation between the gene expression of ICAM-1 and E-selectin and serum levels of diagnostic antibodies (TTG-IgA, TTG-IgG, AGA-IgA, and AGA-IgG) in CD patients. Methodology: A case-control study was conducted involving 124 CD patients and 60 healthy controls. Gene expression of ICAM-1 and E-selectin was quantified using reverse transcription-polymerase chain reaction (RT-PCR), while serum antibody levels were measured via enzyme-linked immunosorbent assay (ELISA). Results: A significant positive correlation was observed between TTG-IgA and TTG-IgG levels (r = 0.85, P < 0.001), whereas AGA-IgA and AGA-IgG exhibited a weak correlation (r = 0.12, P=0.187). ICAM-1 and E-selectin expression was significantly downregulated in CD patients compared to controls (P < 0.001), with a strong positive correlation between the two molecules (r=0.86, P<0.001). ICAM-1 expression demonstrated a moderate positive correlation with antibody levels (P<0.05), suggesting its involvement in immune activation and inflammation in CD. In contrast, E-selectin expression did not significantly correlate with antibody levels, indicating a more complex or indirect role in CD pathogenesis. Conclusion: These findings highlight the potential of ICAM-1 as a biomarker for immune activation in CD and suggest that endothelial adhesion molecules may contribute to disease progression. Further research is warranted to elucidate their precise mechanisms in CD pathogenesis.