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Development and resolution of colitis in mice with target deletion of dipeptidyl peptidase IV (CROSBI ID 185418)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Detel, Dijana ; Pernjak Pugel, Ester ; Batičić Pucar, Lara ; Buljević, Sunčica ; Varljen, Jadranka Development and resolution of colitis in mice with target deletion of dipeptidyl peptidase IV // Experimental physiology, 97 (2012), 4; 486-496. doi: 10.1113/expphysiol.2011.061143

Podaci o odgovornosti

Detel, Dijana ; Pernjak Pugel, Ester ; Batičić Pucar, Lara ; Buljević, Sunčica ; Varljen, Jadranka

engleski

Development and resolution of colitis in mice with target deletion of dipeptidyl peptidase IV

A role for dipeptidyl peptidase IV (DPP IV/CD26) in the pathogenesis of inflammatory bowel disease has been proposed owing to its involvement in immune regulations via its expression on immune cells and ability to cleave biologically active molecules. The aim of the study was to investigate the influence of DPP IV/CD26 deficiency on development and resolution of dextran sulfate sodium-induced colitis in CD26-deficient (CD26-/-) and wild-type (C57BL/6) mice. Colitis was characterized by clinical and histological changes and infiltration of immune cells in colon mucosa. In the acute phase of colitis, loss of body mass and disease activity in C57BL/6 mice was more intensive than in CD26-/- mice, in spite of similar histopathological changes at the local level. Although acute inflammation induced a significant increase in the number of macrophages and dendritic cells in both mouse strains, in CD26-/- mice the increase of macrophages was twice than in C57BL/6 animals (18.0  4.5 vs 41.3  5.8), whereas the increase in dendritic cells was more pronounced in C57BL/6 mice. In the acute phase of colitis, colon DPP IV/CD26 activity was significantly decreased in C57BL/6 mice compared to healthy animals. The results of our study reveal that DPP IV/CD26 deficiency affects the onset of clinical symptoms and the specific cells infiltrating at the site of inflammation in CD26-/- animals, suggesting a pathophysiological role of DPP IV/CD26 and providing new insights into the nature of immune response activated during the development of colitis.

Inflammatory bowel disease; Dextran sulfate sodium-induced colitis; Dipeptidyl peptidase IV/CD26; CD26 deficient mice

Rad je kao poster prezentiran na skupu FEBS 3+ Meeting "From molecules to life and back", održanom od 13.-16.06.2012.g., Opatija, Hrvatska : objavljen u Knjizi sazetaka ; Jerka Dumić, Zrinka Kovarik, Jadranka Varljen (ur.) ; Zagreb : Croatian Society of Biochemistry and Molecular Biology, 2012 ; ISBN 978-953-95551-4-4.

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Podaci o izdanju

97 (4)

2012.

486-496

objavljeno

0958-0670

10.1113/expphysiol.2011.061143

Povezanost rada

Temeljne medicinske znanosti

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