Influence of CD26/dipeptidyl peptidase IV deficiency on immunophenotypic changes during colitis development and resolution

Autor: Sunčica Buljević, Ester Pernjak Pugel, Dijana Detel, Lara Batičić Pučar, Jadranka Varljen, Natalia Kučić
Jazyk: angličtina
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
Pathology
Physiology
Remission
Spontaneous
Biochemistry
Inflammatory bowel disease
0302 clinical medicine
Intestinal mucosa
BIOMEDICINE AND HEALTHCARE. Basic Medical Sciences. Medical Biochemistry
Intestinal Mucosa
Mice
Knockout
Dextran Sulfate
Organ Size
General Medicine
Natural killer T cell
Specific Pathogen-Free Organisms
medicine.anatomical_structure
Liver
Neutrophil Infiltration
Disease Progression
Female
CD26/dipeptidyl peptidase IV
CD26-deficient animals
Dextran sulfate sodium
Immune response
medicine.medical_specialty
Colon
Dipeptidyl Peptidase 4
Spleen
BIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti. Medicinska biokemija
Dipeptidyl peptidase
03 medical and health sciences
Internal medicine
medicine
Animals
Colitis
Dipeptidyl peptidase-4
Peroxidase
business.industry
Transcription Factor RelA
medicine.disease
Mice
Inbred C57BL
Disease Models
Animal
030104 developmental biology
Endocrinology
Gene Expression Regulation
Colitis
Ulcerative
business
Biomarkers
CD8
030215 immunology
Zdroj: Journal of Physiology and Biochemistry
Volume 72
Issue 3
ISSN: 1138-7548
Popis: 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 CD26-deficient 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.
Databáze: OpenAIRE
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