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首页> 外文期刊>World Journal of Gastroenterology >Enhanced plasma ghrelin levels in Helicobacter pylori-colonized, interleukin-1-receptor type 1-homozygous knockout (IL-1R1(-/-)) mice.
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Enhanced plasma ghrelin levels in Helicobacter pylori-colonized, interleukin-1-receptor type 1-homozygous knockout (IL-1R1(-/-)) mice.

机译：增强的幽门螺杆菌定殖的白细胞介素-1水平，白细胞介素-1受体1-纯合敲除（IL-1R1（-/-））小鼠。

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AIM: Ghrelin is an endogenous ligand for the growth hormone secretagogue receptor, and it plays a role in stimulating the growth hormone secretion, food intake, body weight gain and gastric motility. Eradication of Helicobacter pylori (H pylori) was shown to be associated with increase of the body weight. On the other hand, H pylori infection evokes the release of gastric IL-1beta. The present study was designed to investigate the involvement of the gastric IL-1 signal in the ghrelin dynamics in H pylori-colonized mice. METHODS: Twelve-week-old female IL-1-receptor type 1-homozygous-knockout mice (IL-1R1(-/-)) and their wild-type littermates (WT) were orally inoculated with H pylori (Hp group), while other cohorts received oral inoculation of culture medium (Cont group). Thirteen weeks after the inoculation, the mice were examined. The plasma and stomach ghrelin levels and the gastric preproghrelin mRNA were measured. RESULTS: Although the WT mice with H pylori infection showed a significantly decreased body weight as compared with that of the animals without H pylori infection, H pylori infection did not influence the body weight of the IL-1R1-knockout (IL-1R1(-/-)) mice. In the H pylori-infected IL-1R1(-/-) mice, the total and active ghrelin levels in the plasma were significantly increased, and the gastric ghrelin level was decreased. No significant differences were noted in the gastric preproghrelin mRNA expression. CONCLUSION: Ghrelin secretion triggered by H pylori infection might be suppressed by IL-1beta, the release of which is also induced by the infection, resulting in the body weight loss of mice with H pylori infection.
机译：目的：Ghrelin是生长激素促分泌素受体的内源性配体，在刺激生长激素分泌，食物摄入，体重增加和胃蠕动中发挥作用。根除幽门螺杆菌（H pylori）与体重增加有关。另一方面，幽门螺杆菌感染引起胃IL-1β的释放。本研究旨在调查幽门螺杆菌定殖小鼠中胃IL-1信号参与ghrelin动力学。方法：给十二周龄雌性IL-1受体1型纯合敲除小鼠（IL-1R1（-/-））和野生同窝仔（WT）口服幽门螺杆菌（Hp组），其他队列接受了培养基的口服接种（继续组）。接种后十三周，检查小鼠。测量血浆和胃中生长素释放肽水平和胃中前生长激素释放肽mRNA。结果：尽管幽门螺杆菌感染的野生型小鼠与未感染幽门螺杆菌的野生动物相比，体重明显降低，但幽门螺杆菌感染并未影响IL-1R1基因敲除的体重（IL-1R1（- /-）） 老鼠。在幽门螺杆菌感染的IL-1R1（-/-）小鼠中，血浆中总生长素释放肽和活性生长素释放肽水平显着增加，而胃部生长素释放肽水平降低。胃中前proghrelin mRNA表达未发现明显差异。结论：幽门螺杆菌感染引起的Ghrelin分泌可能被IL-1β抑制，IL-1β的释放也被感染诱导，导致幽门螺杆菌感染的小鼠体重减轻。

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