The role of neurogenic inflammation for bacterial translocation

神经源性炎症对细菌易位的作用

• 批准号: 20791323
• 负责人: KOIZUMI Yusuke
• 金额: $ 2.75万
• 依托单位: Shiga University of Medical Science
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20791323/
• 关键词: バクテリアルトランスロケーション; 神経原性炎症; LPS; バニロイド受容体型カチオンチャネル1型(TPRV-1)レセプター

Bacterial translocation is the disease that the pathogen and toxins cross the intestinal barrier systems. It is not a frequent event in healthy people, however, in critically ill patients, bacterial translocation may increase the morbidity and mortality. We investigate the ingression of toxin into intestinal mucosa by using a lipopolysaccharide (LPS). LPS was observed in a particular cell at intestinal mucosa. Intestinal stimulations (inflammation and dilation), furthermore, enhance the bacterial translocation. We will continue further investigations about that phenomenon.

细菌易位是病原体和毒素穿过肠道屏障系统的疾病。这在健康人群中并不常见，但在危重患者中，细菌易位可能会增加发病率和死亡率。我们用脂多糖（LPS）研究了毒素进入肠粘膜的过程。在肠粘膜的特定细胞中观察到LPS。此外，肠道刺激（炎症和扩张）促进了细菌的易位。我们将继续对这一现象进行进一步调查。