动物造模,经肠道播散诱导内源性感染小鼠模型 z-bio 2021-01-15 311

　　OBJECTIVE: To establish a model of diffuse endogenous infection in the intestinal tract of mice, and provide a reliable experimental model for the study of intestinal microecology and related mechanisms of endogenous infection.

　　 Method: 24 ICR female mice were randomly divided into model group A, model group B and control group C, and a broad-spectrum antibiotic solution was given to the model group to destroy the normal intestinal flora. Did you inject 5-fluorouracil (5-FU) from the tail vein for immunosuppression? Is model B based on the introduction of opportunistic pathogens by oral Candida albicans? Is control group C treated with normal saline in the same way? During the experiment, the changes in the fecal flora of the mice were continuously observed, and the mice were detected by the plate counting method. The tissue load and pathological changes of the lung, liver, cecum and colon tissues of the mice were observed by HE staining. The main changes of the mice were observed by the fluorescence quantitative PCR method. Quantitative changes in the intestinal flora?

　　Result: At the end of the experiment, all the tissues and organs of the model group A mice had bacterial infections. Does the model group B mice show mixed infections of bacteria and fungi? The lungs, liver tissues and organs of the two model groups showed typical inflammation, while the cecum and colon showed mucosal inflammation, destroying the integrity of the barrier. The quantitative results of the intestinal flora showed that the structure of the main intestinal flora of the two model groups was disturbed, the resistance to the intestinal flora was reduced, and the B/E value was u003c1?

　　 Conclusion: It indicates the imbalance of intestinal flora and immunosuppression in mice. Then, intestinal or opportunistic pathogens can penetrate the intestinal mucosal barrier and cause tissue and organ infections. From the perspective of intestinal microecology, can this model provide a reliable model basis for the prevention and control of endogenous infections?