Bacterial-induced inflammation in germ-free rabbit appendix.
Bacterial-induced inflammation in germ-free rabbit appendix.
复制标题
无菌兔阑尾细菌引起的炎症。
DOI：
10.1097/01.mib.0000182869.74648.0f
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发表时间：
2005
影响因子：
4.9
通讯作者：
Knight,KatherineL
中科院分区：
文献类型：
--
作者：
Shanmugam,Malathy;Sethupathi,Periannan;Rhee,Ki-Jong;Yong,Sherri;Knight,KatherineL
肠道生态系统由微生物群、粘膜上皮和肠道相关淋巴组织（GALT）之间的一系列相互作用定义。这些组分之间相互作用的精细平衡的扰动可导致胃肠道疾病，如炎症性肠病（IBD）。IBD的病理生理学被认为是由于对正常管腔微生物群落的粘膜免疫应答失调而发展的。已经开发了几种IBD的动物模型，并强调了免疫系统在疾病发展中的作用。大多数研究IBD的现有动物模型是基于使用化学诱导的IBD或遗传修饰和无菌动物。然而，重要的是要研究炎症反应，可以从细菌之间的相互作用，粘膜上皮细胞，和GALT在动物，没有遗传修饰或免疫功能低下。在这份报告中，我们记录了使用无菌结扎兔阑尾模型诱导炎症反应的变化，以特定的细菌。将人类的普通拟杆菌引入无菌结扎的阑尾后，我们发现了慢性炎症变化，包括腺体变形、腺体脱落、杯状细胞减少和隐窝脓肿形成。然而，随着其他实验管腔内容物的引入，我们没有观察到炎症。这些结果表明，特定的微生物组合物可以诱导炎症。我们认为，该模型可能有助于研究特定细菌在肠道中建立炎症反应的机制。
The intestinal ecosystem is defined by a series of interactions between the microbiota, the mucosal epithelium, and the gut-associated lymphoid tissue (GALT). Perturbations in the fine balance of the interactions between these components can result in gastrointestinal diseases such as inflammatory bowel disease (IBD). The pathophysiology of IBD is thought to develop as a result of dysregulated mucosal immune responses to normal luminal microflora. Several animal models for IBD have been developed and underscore the role of the immune system in development of disease. Most of the existing animal models studying IBD are based on the use of chemically induced IBD or of genetically modified and germ-free animals. It is, however, important to study inflammatory responses that can develop from interactions between bacteria, the mucosal epithelium, and GALT in animals that are not genetically modified or immunocompromised. In this report, we document the use of a germ-free ligated rabbit appendix model to induce inflammatory changes in response to specific bacteria. With the introduction of aBacteroides vulgatusisolate from humans into the germ-free ligated appendix, we found chronic inflammatory changes, including glandular distortion, gland drop-out, decreased goblet cells, and crypt abscess formation. However, with the introduction of other experimental luminal contents, we observed no inflammation. These results show that specific microbial composition can induce inflammation. We suggest that this model may be useful to study the mechanism by which specific bacteria establish inflammatory responses in the gut.