Influence of CD26/dipeptidyl peptidase IV deficiency on immunophenotypic changes during colitis development and resoluti
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ORIGINAL PAPER
Influence of CD26/dipeptidyl peptidase IV deficiency on immunophenotypic changes during colitis development and resolution Dijana Detel & Suncica Buljevic & Lara Baticic Pucar & Natalia Kucic & Ester Pernjak Pugel & Jadranka Varljen Received: 3 June 2015 / Accepted: 20 April 2016 # University of Navarra 2016
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 (DSS)-induced colitis in wild-type (WT) and CD26-deficient mice. Development of clinical symptoms of colitis and animal health status parameters were assessed; the expression of the nuclear factor (NF)-κB p65 subunit was measured by quantitative real-time 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 CD26-deficient mice was more intensive than in WT mice, in spite of similar histopathological changes. Furthermore, a significant increase in the expression of NF-κB p65 subunit in the colon of CD26-deficient 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 CD26-deficient 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 NF-κB p65 subunit and distinct changes in leukocyte trafficking. These results provide new insights into the role of CD26/DPP IV during the development of colitis. Keywords Inflammatory bowel disease . CD26/ dipeptidyl peptidase IV . CD26-deficient animals . Dextran sulfate sodium . Immune response
Introduction (*) : S. Buljevic : L. B. Pucar : J. Varljen
D. Detel Department of Chemistry and Biochemistry, School of Medicine, University of Rijeka, Braće Branchetta 20, HR-51000 Rijeka, Croatia e-mail: [email protected] N. Kucic Department of Physiology and Immunology, School of Medicine, University of Rijeka, Rijeka, Croatia E. P. Pugel Department of Histology and Embryology, School of Medicine, University of Rijeka, Rijeka, Croatia
Inflammatory bowel disease (IBD) comprise two chronic inflammatory diseases of humans, namely ulcerative colitis (UC) and Crohn’s disease. They are both spontaneously relapsing, immunologically mediated disorders characterized by a variety of symptoms, depending on the disease extent and severity. Despite intense research, the exact etiology and pathogenesis of these disorders has remained e
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