The role of estrogen signaling in a mouse model of inflammatory bowel disease: a Helicobacter hepaticus model.
The role of estrogen signaling in a mouse model of inflammatory bowel disease: a Helicobacter hepaticus model.
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DOI：
10.1371/journal.pone.0094209
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Franklin CL
中科院分区：
文献类型：
--
作者：
Cook LC;Hillhouse AE;Myles MH;Lubahn DB;Bryda EC;Davis JW;Franklin CL
炎症性肠病（IBD）、克罗恩病和溃疡性结肠炎的发病机制部分是由于免疫系统、遗传、环境和内源性微生物群之间的相互作用。生殖腺性激素（GSH），如雌激素，被认为与IBD的发展有关，因为疾病严重程度的变化发生在怀孕、更年期或口服避孕药的使用期间。在某些小鼠品系中，感染肝螺杆菌会引发ibd样粘膜炎症，雌性小鼠比雄性小鼠更严重，提示谷胱甘肽在该模型中发挥作用。为了确定雌激素信号在微生物诱导的肠道炎症中的作用，我们使用了雌激素受体(ER) α和β敲除（KO）小鼠、ER激动剂和过继转移。我们证明，当信号仅限于非cd4 +细胞亚群上的ERβ时，疾病不那么严重，这与促炎介质的表达减少有关。
The pathogenesis of inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis, is due in part to interactions between the immune system, genetics, the environment, and endogenous microbiota. Gonadal sex hormones (GSH), such as estrogen, are thought to be involved in the development of IBD as variations in disease severity occur during pregnancy, menopause, or oral contraceptives use. In certain strains of mice, infection with Helicobacter hepaticus triggers IBD-like mucosal inflammation that is more severe in female mice than in males, suggesting a role for GSH in this model. To determine the role of estrogen signaling in microbiota-induced intestinal inflammation, estrogen receptor (ER) α and β knock-out (KO) mice, ER agonists, and adoptive transfers were utilized. We demonstrate that, when signaling is limited to ERβ on a non-CD4+ cell subset, disease is less severe and this correlates with decreased expression of pro-inflammatory mediators.
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影响因子：
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DOI：
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