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Correlation of Serum Vitamin A Levels with Disease Activity Indices and Colonic IL ‐23R and FOXP 3 mRNA Expression in Ulcerative Colitis Patients
Author(s) -
Verma P.,
Subodh S.,
Tiwari V.,
Rampal R.,
Tuteja A.,
Toteja G. S.,
Gupta S. D.,
Ahuja V.
Publication year - 2016
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12450
Subject(s) - ulcerative colitis , disease , pathogenesis , medicine , downregulation and upregulation , immunology , gastroenterology , biology , gene , genetics
Genome‐wide association studies have identified IL ‐23 receptor ( IL ‐23R) as a susceptibility locus for the pathogenesis of ulcerative colitis ( UC ), which is characterized by exaggerated Th2/Th17 response. Studies have shown that vitamin A ( VA ) reduces disease progression by promoting FOXP 3⁺ T cells and curbing Th17 cells. In this study, we explored the association of colonic IL ‐23R and FOXP 3 expression in fifty‐one UC patients (23 in remission and 28 with active disease) with serum VA levels and disease activity. We observed that decreased serum VA levels were associated with increased disease activity. However, there was no significant difference in mucosal IL ‐23R and FOXP 3 expression in UC patients with moderate–to‐severe disease activity compared to those in remission. Also, no significant correlation was drawn between serum VA levels and mucosal IL ‐23R and FOXP 3 expression. Our study suggests that even after an established role of VA in inhibiting Th17 responses in mice models and humans, serum VA levels and disease activity do not correlate with FOXP 3 and IL ‐23R expression in colonic mucosa of UC patients.