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细菌从胃肠道的移位。

Bacterial translocation from the gastrointestinal tract.

作者信息

Berg R D

机构信息

Department of Microbiology and Immunology, Louisiana State University Medical School, Louisiana State University Medical Center-Shreveport 71130.

出版信息

J Med. 1992;23(3-4):217-44.

PMID:1479301
Abstract

Bacterial translocation is defined as the passage of viable bacteria from the gastrointestinal tract to extraintestinal sites, such as the mesenteric lymph node complex, liver, spleen, kidney, and blood. The major mechanisms promoting bacterial translocation in animal models are: (a) disruption of the ecologic equilibrium to allow intestinal bacterial overgrowth, (b) deficiencies in host immune defenses, and (c) increased permeability of the intestinal mucosal barrier. These mechanisms can act in concert to promote synergistically the systemic spread of indigenous translocating bacteria to cause lethal sepsis. Studies are presented of attempts to delineate the mechanisms promoting bacterial translocation utilizing animal models of intestinal bacterial overgrowth, immunosuppression, T-cell deficiencies, solid tumors, leukemia, diabetes, endotoxemia, hemorrhagic shock, thermal injury, bowel obstruction, bile duct ligation, protein malnutrition and parenteral nutrition. Also described are the use of selective antibiotic decontamination or nonspecific macrophage immunomodulators in attempts to reduce bacterial translocation from the gastrointestinal tract.

摘要

细菌移位被定义为活细菌从胃肠道转移至肠外部位,如肠系膜淋巴结复合体、肝脏、脾脏、肾脏及血液。在动物模型中促进细菌移位的主要机制包括:(a)生态平衡破坏导致肠道细菌过度生长;(b)宿主免疫防御缺陷;(c)肠道黏膜屏障通透性增加。这些机制可协同作用,促进内源性移位细菌的全身播散,引发致死性败血症。本文介绍了利用肠道细菌过度生长、免疫抑制、T细胞缺陷、实体瘤、白血病、糖尿病、内毒素血症、失血性休克、热损伤、肠梗阻、胆管结扎、蛋白质营养不良及肠外营养等动物模型来阐明促进细菌移位机制的研究。还描述了使用选择性抗生素去污或非特异性巨噬细胞免疫调节剂来试图减少胃肠道细菌移位的情况。

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