Macrophages are mediators of gastritis in acute Helicobacter pylori infection in C57BL/6 mice
Macrophages are mediators of gastritis in acute Helicobacter pylori infection in C57BL/6 mice
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DOI：
10.1128/iai.01481-07
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发表时间：
2008-05-01
影响因子：
3.1
通讯作者：
Strugnell, Richard A.
中科院分区：
文献类型：
--
作者：
Kaparakis, Maria;Walduck, Anna K.;Strugnell, Richard A.
幽门螺杆菌是人类慢性胃炎的病原体，慢性胃炎被视为胃肠道溃疡或胃癌发展的先兆。本研究利用慢性幽门螺杆菌感染的小鼠模型来表征巨噬细胞在诱导特异性免疫反应和胃炎以及控制幽门螺杆菌感染和疫苗接种后的细菌负荷中的作用。静脉注射载药脂质体以消耗C57BL/6小鼠的巨噬细胞，并通过免疫荧光显微镜证实有效去除小鼠脾和胃中的CD11b(+)细胞。在感染早期从 C57BL/6 小鼠中瞬时消除巨噬细胞可减少幽门螺杆菌 SS1 诱导的胃病理，但不影响胃中的细菌负荷。这些数据表明巨噬细胞对于幽门螺杆菌感染期间胃部炎症的严重程度很重要。
Helicobacter pylori is the etiological agent of human chronic gastritis, a condition seen as a precursor to the development of gastrointestinal ulcers or gastric cancer. This study utilized the murine model of chronic H. pylori infection to characterize the role of macrophages in the induction of specific immune responses and gastritis and in the control of the bacterial burden following H. pylori infection and vaccination. Drug-loaded liposomes were injected intravenously to deplete macrophages from C57BL/6 mice, and effective removal of CD11b(+) cells from the spleens and stomachs of mice was confirmed by immunofluorescence microscopy. Transient elimination of macrophages from C57BL/6 mice during the early period of infection reduced the gastric pathology induced by H. pylori SS1 but did not affect the bacterial load in the stomach. These data suggest that macrophages are important to the severity of gastric inflammation during H. pylori infection.