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https://doi.org/10.5562/cca1813

Relevance of DPP IV/CD26 among the Gut-brain Axis during Experimental Colitis

Lara Batičić Pučar ; Department of Chemistry and Biochemistry, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia
Dijana Detel ; Department of Chemistry and Biochemistry, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia
Sunčica Buljević ; Department of Chemistry and Biochemistry, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia
Ester Pernjak Pugel ; Department of Histology and Embriology, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia
Natalia Kučić ; Department of Physiology and Immunology, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia
Jadranka Varljen ; Department of Chemistry and Biochemistry, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia


Puni tekst: engleski pdf 5.022 Kb

str. 201-208

preuzimanja: 1.010

citiraj


Sažetak

Inflammatory bowel diseases (IBD) represent a group of chronic conditions of the gastrointestinal
tract of unknown etiology. Latest knowledge accentuates the bidirectional connection between the central and
enteric nervous systems. An important role of peptidases has been proposed in maintaining the homeostasis
in the gut. One of them is dipeptidil-peptidase IV (DPP IV/CD26), a multifunctional glycoprotein found in
both soluble and membrane-bound form in living organisms. In order to evaluate the relevance of DPP
IV/CD26 among the gut-brain axis, a TNBS (Crohn-like) model of colitis has been induced in CD26 deficient
and wild type mice. Results of this study showed that CD26 deficient mice show specificity in histological
damage compared to wild type mice. A decreased DPP IV/CD26 activity was found in serum, colon and
brain in wild type mice with colitis, while CD26 protein expression was increased in colon of those mice.
DPP IV/CD26-like activity was decreased only in colon of CD26 deficient mice. Changes occurring during
inflammatory processes in colon reflected on investigated parameters in brain. Therefore, our results indicate
the importance of the gut-brain axis in the pathogenesis of IBD. (doi: 10.5562/cca1813)

Ključne riječi

dipeptidyl-peptidase IV; CD26 molecule; CD26 deficient mice; inflammatory bowel diseases; TNBS-colitis; gut-brain axis

Hrčak ID:

84537

URI

https://hrcak.srce.hr/84537

Datum izdavanja:

11.5.2012.

Posjeta: 1.754 *