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Macrophages Are Mediators of Gastritis in Acute Helicobacter pylori Infection in C57BL/6 Mice

机译:巨噬细胞是C57BL / 6小鼠急性幽门螺杆菌感染中胃炎的介导者。

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摘要

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.
机译:幽门螺杆菌是人类慢性胃炎的病原体,被认为是胃肠道溃疡或胃癌发展的前兆。这项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定的免疫反应和胃炎以及控制幽门螺杆菌感染和接种疫苗后细菌负担中的作用。静脉注射载有药物的脂质体以耗尽C57BL / 6小鼠的巨噬细胞,并通过免疫荧光显微镜检查确认了小鼠脾脏和胃中CD11b + 细胞的有效去除。在感染早期从C57BL / 6小鼠中瞬时清除巨噬细胞可减轻幽门螺杆菌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幽门螺杆菌感染期间胃炎症的严重性很重要。

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