Abstract

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.

Highlights

  • Intestinal microbiota is the largest and most diverse community of microorganisms in the human body

  • While the exposure of mice from group at mice exposed to 5% DSS (AM5) to 5% dextran sodium sulphate (DSS) had a negative influence on the viability of microorganisms in the cecal content, exposure to 3% and 1% concentrations of DSS failed to produce a marked negative influence on the viability of cecal microbiota in groups AM3 and AM1, where it varied at 84.7 ± 0.55% and 73.57 ± 3.5%, respectively

  • The obtained pseudo germ-free (PGF) model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the inflammatory process developed mostly due to the exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine

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Summary

Introduction

Intestinal microbiota is the largest and most diverse community of microorganisms in the human body. The symbiotic relationship between intestinal microbiota and the host is regulated and. Cells 2020, 9, 2571 stabilized by a complex network of interactions that include metabolic, immune, and neuroendocrine relationships among them [1]. The pathologically unimpaired intestinal microbiota acts symbiotically, produces vitamins, suppresses expansion of pathological microorganisms and facilitates digestion of food substrates while constantly interacts with the immune system of the host. The more abundant and diverse the microbiota turns in the course of life the better the organism will resist to attacks from the outer environment. Intestinal microbiota constitutes a changing ecosystem considerably burdened by many factors, such as unbalanced food, stress, use of antibiotics, or suffering from diseases [2]

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