Influence of CD26/dipeptidyl peptidase IV deficien

Authors: Dijana Detel Suncica Buljevic Lara Baticic Pucar Natalia Kucic Ester Pernjak Pugel Jadranka Varljen

Publish Date: 2016/04/28

Volume: 72, Issue: 3, Pages: 405-419

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Abstract

A lot of evidence for the importance of CD26/dipeptidyl peptidase IV CD26/DPP IV in immunoactivation has been reported however its involvement in colitis remains unclear The aim of this study was to investigate the influence of CD26/DPP IV deficiency on immunophenotypic changes associated with dextran sulfate sodium DSSinduced colitis in wildtype WT and CD26deficient mice Development of clinical symptoms of colitis and animal health status parameters were assessed the expression of the nuclear factor NFκB p65 subunit was measured by quantitative realtime PCR while cell characterization was determined by flow cytometry and immunohistochemical staining DSS treatment induced loss of body weight and colon length shortening in both mouse strains An increase of myeloperoxidase activity in CD26deficient mice was more intensive than in WT mice in spite of similar histopathological changes Furthermore a significant increase in the expression of NFκB p65 subunit in the colon of CD26deficient mice was determined The percentage of splenic CD4+ and CD8+ cells in the acute phase of colitis was significantly decreased in WT mice while in the same period an increase in the percentage of splenic CD8+ cells was present in CD26deficient mice Development of colitis was accompanied by a significant increase in the percentage of intrahepatic NKT cells in both mouse strains but their percentage in spleen was increased only in CD26deficient mice CD26 deficiency was associated with a heightened response to DSS accompanied by increased expression of NFκB p65 subunit and distinct changes in leukocyte trafficking These results provide new insights into the role of CD26/DPP IV during the development of colitisThe research was supported by the Ministry of Science Education and Sports of the Republic of Croatia grant no 06200612450213 and University of Rijeka grant no 13061226 We gratefully acknowledge Professor Didier Marguet Centre d’Immunologie de MarseilleLuiny Université de la Méditerrance Marseille France for providing CD26deficient animals The authors wish to thank Ioannis Pateras MD PhD Department of Histology National and Kapodistrian University of Athens Greece for performing p65 immunohistochemical staining as well as the head of the Department Professor Vassilis Gorgoulis for his affability We kindly thank Professor Siniša Volarević Department of Molecular Biology School of Medicine University of Rijeka Croatia for continuous support and collaboration through the TransMedRi project and Professor Stipan Jonjić for allowing us to use all the facilities of the Department of Histology and Embryology School of Medicine University of Rijeka Croatia The authors would like to thank Tihana and Ben Harrison for valuable language suggestions

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