Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice

被引:36
|
作者
Gancarcikova, Sona [1 ]
Lauko, Stanislav [1 ]
Hrckova, Gabriela [2 ]
Andrejcakova, Zuzana [3 ]
Hajduckova, Vanda [1 ]
Madar, Marian [1 ]
Fecskeova, Livia Kolesar [4 ]
Mudronova, Dagmar [1 ]
Mravcova, Kristina [5 ]
Strkolcova, Gabriela [5 ]
Nemcova, Radomira [1 ]
Kacirova, Jana [1 ]
Staskova, Andrea [6 ]
Vilcek, Stefan [5 ]
Bomba, Alojz [7 ]
机构
[1] Univ Vet Med & Pharm Kosice, Dept Microbiol & Immunol, Kosice 04181, Slovakia
[2] Slovak Acad Sci, Inst Parasitol, Kosice 04181, Slovakia
[3] Univ Vet Med & Pharm Kosice, Dept Biol & Physiol, Kosice 04181, Slovakia
[4] Czech Acad Sci, Ctr Algatech, Inst Microbiol, Trebon 37901, Czech Republic
[5] Univ Vet Med & Pharm Kosice, Dept Epizootol Parasitol & Protect One Hlth, Kosice 04181, Slovakia
[6] Pavol Jozef Safarik Univ Kosice, Dept Stomatol & Maxilofacial Surg, Kosice 04181, Slovakia
[7] Pavol Jozef Safarik Univ Kosice, Fac Med, Inst Expt Med, Kosice 04181, Slovakia
关键词
pseudo germ-free model; antibiotics; DSS-induced colitis; gut microbiota; histopathology; DEXTRAN SULFATE SODIUM; REGULATORY T-CELLS; CHAIN FATTY-ACIDS; ANTIBIOTIC-TREATMENT; GUT MICROBIOTA; INTESTINAL INFLAMMATION; BACTERIA; METABOLITES; DYSBIOSIS; DISEASE;
D O I
10.3390/cells9122571
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.
引用
收藏
页码:1 / 28
页数:28
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