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首页> 外文期刊>Infection and immunity >Role for Complement in Development of Helicobacter-Induced Gastritis in Interleukin-10-Deficient Mice
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Role for Complement in Development of Helicobacter-Induced Gastritis in Interleukin-10-Deficient Mice

机译：在白介素10缺陷型小鼠中由幽门螺杆菌诱导的胃炎的发生中的补体作用

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The mechanisms by which the immune response can eradicate gastric Helicobacter infection are unknown. We hypothesized that Helicobacter-induced activation of the complement system could promote both inflammation and eradication of Helicobacter from the stomach. In vitro studies demonstrated that Helicobacter felis activates complement in normal mouse serum but not in serum from Rag2?/? mice, indicating that H. felis activates complement through the classical pathway. Next, we infected complement-depleted wild-type control and interleukin-10-deficient (IL-10?/?) mice with H. felis. Helicobacter infection of wild-type mice elicited a mild, focal gastritis and did not alter serum complement levels. Infection of IL-10?/? mice with H. felis elicited severe gastritis. After the initial colonization, the IL-10?/? mice completely cleared Helicobacter from the stomach by day 8. In contrast to wild-type mice, H. felis-infected IL-10?/? mice had a marked increase in serum complement levels. Complement depletion of wild-type mice did not affect the intensity of gastric inflammation or the extent of Helicobacter colonization compared to that for the wild-type control mice. In contrast, complement depletion of Helicobacter-infected IL-10?/? mice decreased the severity of gastritis, decreased the Helicobacter-induced infiltration of neutrophils into the stomach, and delayed the clearance of bacteria. In vitro studies of stimulated splenocytes and neutrophils from IL-10?/? mice produced a twofold increase in complement production compared to that for wild-type mice. Pretreatment with IL-10 inhibited this increase. These studies identify a role for complement in the local immune response to gastric Helicobacter in IL-10?/? mice and suggest a role for IL-10 in the regulation of complement production.
机译：免疫反应消除胃 Helicobacter 感染的机制尚不清楚。我们假设幽门螺杆菌诱导的补体系统激活可以促进胃部炎症和根除幽门螺杆菌。体外研究表明，幽门螺杆菌激活正常小鼠血清中的补体，但不能激活Rag2 α/？小鼠血清中的补体，表明 H。 felis 通过经典途径激活补体。接下来，我们用 H感染缺乏补体的野生型对照和白介素10缺陷型（IL-10 ？/？）小鼠。费利斯。野生型小鼠的幽门螺杆菌感染可引起轻度局灶性胃炎，并且不会改变血清补体水平。 IL-10 ？/？小鼠感染 H。 felis 引起严重的胃炎。最初定植后，IL-10 ？/？小鼠在第8天时已完全从胃中清除了 Helicobacter 。与野生型小鼠相比， H。感染猫的IL-10 ？/？小鼠的血清补体水平明显升高。与野生型对照小鼠相比，野生型小鼠的补体耗竭不会影响胃部炎症的强度或幽门螺杆菌的定殖程度。相反，感染幽门螺杆菌的IL-10 ？/？小鼠的补体耗竭降低了胃炎的严重程度，降低了幽门螺杆菌引起的胃粘膜浸润中性粒细胞进入胃，并延迟了细菌的清除。与野生型小鼠相比，对来自IL-10 α/β小鼠的刺激的脾细胞和嗜中性白细胞的体外研究使补体产生增加了两倍。 IL-10预处理抑制了这种增加。这些研究确定了补体在IL-10 ？/？小鼠中对胃幽门螺杆菌的局部免疫反应中的作用，并暗示了IL-10在补体调节中的作用。生产。

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