动物造模 z-bio 2022-09-13 445

　　Objective: To establish a mouse model of endogenous infection induced by intestinal dissemination, and to provide a reliable experimental model for studying the mechanism of intestinal microecology and endogenous infection.

　　Methods: Twenty-four ICR female mice were randomly divided into model group A, model group B and control group C. Model group A was given a broad-spectrum antibiotic solution orally to destroy normal intestinal flora, and then was injected with 5-fluorouracil (5-FU) via tail vein. Immunosuppression was performed. On the basis of model group A, Candida albicans was given by gavage to introduce opportunistic pathogens, which is model group B. Control group C was treated with normal saline in the same way. During the experiment, the fecal bacteria of mice were continuously observed. The bacterial population of mice was detected by plate counting method, the pathological changes of lung, liver, cecum and large intestine of mice were observed by HE staining, and the quantitative changes of main intestinal flora of mice were observed by fluorescence quantitative PCR method.

　　Results: At the end of the experiment, the tissues and organs of model group A mice were all infected with bacteria, while model group B mice showed mixed infection of bacteria and fungi. The lung and liver tissues and organs of the two model groups showed typical inflammation, while the cecum showed typical inflammation. The intestinal microflora and the large intestine were characterized by mucosal inflammation and destruction of barrier integrity. The quantitative results of intestinal flora showed that the structure of the main intestinal flora in the two model groups was disordered, and the intestinal colonization resistance decreased, and the B/E value was less than 1.

　　Conclusion: Under the condition of intestinal flora disorder and immunosuppression in mice, intestinal pathogens or opportunistic pathogens break through the intestinal mucosal barrier and cause tissue and organ infection. This model can be used for the prevention and control of intestinal microecology. The study of endogenous infection provides a reliable model basis.