[Animal modeling] - Establishment and evaluation of a mouse model of endogenous infection induced by intestinal dissemination

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

  Methods: 24 female ICR mice were randomly divided into model group A, model group B and control group C. Model group A was given broad-spectrum antibiotic solution orally to destroy the normal intestinal flora and then injected 5-fluorouracil (5-FU) into tail vein Immunosuppression was carried out. On the basis of model group A, Candida albicans was given by gavage to introduce opportunistic pathogens, which is model group B. The control group C was treated with normal saline in the same way. During the experiment, the changes of fecal flora of mice were continuously observed, the bacterial load of mouse tissues was detected by plate counting, the pathological changes of mouse lung, liver, cecum and large intestine were observed by HE staining, and the quantitative changes of main intestinal flora of mice were observed by fluorescence quantitative PCR

  Results: At the end point of the experiment, the tissues and organs of mice in model group A were infected with bacteria, and mice in model group B were infected with bacteria and fungi. The lung and liver tissues and organs of mice in the two model groups showed typical inflammation, while the cecum and large intestine showed mucosal inflammation and the integrity of the barrier was destroyed. The quantitative results of intestinal flora showed that the structure of the main intestinal flora in the two model groups was disordered, 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 pathogenic bacteria or opportunistic pathogenic bacteria break through the intestinal mucosal barrier and cause tissue and organ infection. This model can provide a reliable model basis for the research on prevention and control of endogenous infection from the aspect of intestinal microecology