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首页> 外文期刊>Comparative Medicine >Sex influence on chronic intestinal inflammation in Helicobacter hepaticus-infected A/JCr mice
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Sex influence on chronic intestinal inflammation in Helicobacter hepaticus-infected A/JCr mice

机译：性别对感染Helicobacter hepaticus的A / JCr小鼠的慢性肠道炎症的影响

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Helicobacter hepaticus is a bacterial pathogen of mice that has been reported to cause chronic intestinal inflammation in A/JCr, germfree Swiss Webster, and immunodeficient mice. To the authors' knowledge, the influence of sex on development of chronic intestinal inflammation in H. hepaticus-infected mice has not been investigated. The purposes of the study reported here were to determine whether severity of intestinal inflammation differs between male and female A/JCr mice chronically infected with H. hepaticus and to characterize the mucosal immune response in these mice. The cecum of male and female A/JCr mice infected with H. hepaticus for 1 month and 3 months was objectively evaluated histologically for intestinal disease. Also, semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) analysis was done to measure interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin 4 (IL-4), IL-10, macrophage inflammatory protein-1alpha (MIP-1alpha), interferon-inducible protein of 10 kDa (IP-10), and monokine induced by gamma interferon (MIG) mRNA values in the cecal tissue of these mice. Significant differences in cecal lesion scores were not present at 1 month after infection. However, infected female mice had significantly up-regulated expression of cecal IL-10, MIP-1a, IP-10, and MIG mRNA compared with that in uninfected females, and expression of IL-10 and MIP-1alpha was significantly greater than that detected in infected male mice (P less than or equal to 0.05). At 3 months after infection, cecal lesion scores were significantly (P: 0.05) increased in female and male mice compared with uninfected controls, and infected female mice had significantly (P: 0.05) higher cecal lesion scores than did infected male mice. In addition, infected females had significant (P less than or equal to 0.05) increases in cecal IFN-gamma, TNF-alpha, IL-10, MIP-1alpha, IP-10, and MIG mRNA values compared with values in uninfected females and infected males, and male mice had significant (P: 0.05) increases in cecal TNF-a and IL-10 mRNA values compared with those for male control mice. These data indicate that, in H. hepaticus-infected A/JCr mice, females develop more severe intestinal inflammation than do males, and the chronic mucosal inflammation is polarized toward a Th1 response that is not down-regulated by increased activity of IL-10. We propose that H. hepaticus-infected A/JCr mice will serve as a good animal model with which to study the influence of sex on bacterial-induced mucosal inflammation.
机译：肝幽门螺杆菌是小鼠的细菌病原体，据报道会引起A / JCr，无菌Swiss Webster和免疫缺陷小鼠的慢性肠道炎症。据作者所知，尚未研究性别对感染H. hepaticus的小鼠中慢性肠道炎症发展的影响。此处报道的研究目的是确定慢性感染肝炎的雄性和雌性A / JCr小鼠之间肠道炎症的严重程度是否有所不同，并表征这些小鼠的粘膜免疫反应。从组织学上客观地评估了感染了H. hepaticus的雄性和雌性A / JCr小鼠的盲肠的肠道疾病。此外，还进行了半定量逆转录聚合酶链反应（RT-PCR）分析，以测量干扰素-γ（IFN-γ），肿瘤坏死因子-α（TNF-alpha），白介素4（IL-4），IL -10，巨噬细胞炎性蛋白-1α（MIP-1alpha），10 kDa的干扰素诱导蛋白（IP-10）以及这些小鼠的盲肠组织中由γ干扰素（MIG）mRNA值诱导的单因子。感染后1个月，盲肠病变评分无明显差异。然而，与未感染的雌性小鼠相比，感染的雌性小鼠的盲肠IL-10，MIP-1a，IP-10和MIG mRNA的表达明显上调，并且IL-10和MIP-1alpha的表达明显高于未感染的雌性。在感染的雄性小鼠中检测到（P小于或等于0.05）。感染后3个月，雌性和雄性小鼠的盲肠病变得分显着（P：0.05）与未感染的对照组相比明显升高，并且感染的雌性小鼠的盲肠病变得分显着高于感染的雄性小鼠（P：0.05）。此外，与未感染的女性和未感染女性相比，受感染的女性盲肠IFN-γ，TNF-alpha，IL-10，MIP-1alpha，IP-10和MIG mRNA的值显着增加（P小于或等于0.05）。感染的雄性，与雄性对照组相比，雄性小鼠的盲肠TNF-a和IL-10 mRNA值显着增加（P：0.05）。这些数据表明，在感染肝炎的A / JCr小鼠中，雌性小鼠比男性更严重的肠道炎症，并且慢性粘膜炎症朝着Th1反应极化，而Th1反应并未被IL-10活性的增加下调。 。我们建议，感染H. hepaticus的A / JCr小鼠将作为研究动物性别对细菌诱导的粘膜炎症影响的良好动物模型。

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