P046 CD99 and cyclophilin A correlate differently in patients with inflammatory bowel diseases
M. Wlodarczyk*1, A. Sobolewska1, M. Cichalewska2, J.-P. Timmermans3, K. Stec-Michalska1, M. Mycko2, J. Fichna4, M. Wisniewska-Jarosinska1, A. Piechota-Polanczyk4
1Medical University of Lodz, Department of Gastroenterology, Lodz, Poland, 2Medical University of Lodz, Laboratory of Neuroimmunology, Department of Neurology, Lodz, Poland, 3University of Antwerp, Laboratory of Cell Biology and Histology, Department of Veterinary Sciences, Antwerp, Belgium, 4Medical University of Lodz, Department of Biochemistry, Lodz, Poland
Inflammatory bowel diseases (IBD) are characterized by crypt infiltration with neutrophils, which can be stimulated by externalization of an adhesion molecule CD99. Neutrophil infiltration is associated with upregulation of cyclophilin A (CyPA). However, studies on CD99 and CyPA in IBD patients have not been performed yet. The aim of the study was to determine the CD99 gene and protein expression and extra- and intracellular concentration of CyPA in UC and CD patients in comparison to healthy subjects.
Correlations between CD99 and CyPA in non-inflamed and inflamed colon areas in UC and CD patients.
|UC / r^2 / Gene level||UC / r^2 / Protein level||CD / r^2 / Gene level||CD / r^2 / Protein level|
|CyPA [ng/ml] in plasma vs. CD99 in non-inflamed colon areas||+0.770||+0.530||-0.651||-0.274|
|CyPA [ng/ml] in plasma vs. CD99 in inflamed colon areas||-0.535||+0.090||-0.344||-0.478|
|CyPA [ng/ml] in non-inflamed vs. CD99 in non-inflamed colon areas||-0.580||-0.086||-0.357||-0.756|
|CyPA [ng/ml] in inflamed vs. CD99 in inflamed colon areas||+0.796||+0.488||+0.436||-0.333|
The study incorporated 26 patients divided into: control (n=7), UC (n=7) and CD (n=12). The patients were matched by age and gender. The samples comprised serum and colonoscopy biopsies from non-inflamed and inflamed (in UC or CD) colon areas. The CD99 mRNA was analysed by RT-PCR, and CD99 and CyPA protein levels by immunoenzymatic Methods (ELISA and Western blot).
The UC patients had significantly lower CD99 mRNA in non-inflamed tissue and higher in inflamed colon areas comparing to CD (p=0.035 and p=0.021, respectively). The extracellular CyPA level was 4.6- and 2.8-times higher in UC and CD than in control (p=0.017 and p=0.137, respectively). CyPA was significantly lower in non-inflamed tissue in the CD group compared to control (p=0.039). Reversed correlations were found between CyPA and CD99 in inflamed tissues of CD and UC patients.
Our study indicated that patients with UC had increased level of CD99 and CyPA both in plasma and tissue. Moreover, CD99 gene expression correlated inversely with intracellular CyPA level in inflamed and non-inflamed colon tissue in UC, but not CD. We suggest that there may be a link between CD99 and CyPA in IBD etiology. It is likely that CD99-CyPA interaction influences the inflammatory process in colitis, as in our study both CD99 and CyPA were increased in inflamed colon areas from UC patients. However, further studies are necessary to confirm those observations and to describe how, if at all, CyPA releasing influences CD99 signaling in IBD.