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黏膜细胞因子谱失衡导致动物首次接触粪便细菌和抗原后出现短暂的肠道炎症。

An imbalance in mucosal cytokine profile causes transient intestinal inflammation following an animal's first exposure to faecal bacteria and antigens.

机构信息

Center of Excellence for Gastrointestinal Inflammation and Immunity Research, Division of Gastroenterology, Department of Medicine, University of Alberta, Edmonton, AB, Canada.

出版信息

Clin Exp Immunol. 2010 Jul 1;161(1):187-96. doi: 10.1111/j.1365-2249.2010.04140.x. Epub 2010 Mar 16.

Abstract

Intestinal microflora play a critical role in the initiation and perpetuation of chronic inflammatory bowel diseases. In genetically susceptible hosts, bacterial colonization results in rapid-onset chronic intestinal inflammation. Nevertheless, the intestinal and systemic immune response to faecal bacteria and antigen exposure into a sterile intestinal lumen of a post-weaned animal with a mature immune system are not understood clearly. This study examined the effects of faecal bacteria and antigen exposure on the intestinal mucosal and systemic immune system in healthy axenic mice. Axenic wild-type mice were inoculated orally with a crude faecal slurry solution derived from conventionally raised mice and were analysed prior to and then at days 3, 7, 14 and 28 post-treatment. Ingestion of faecal slurry resulted in a transient, early onset of proinflammatory interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and interleukin (IL)-17 response that was maximal at day 3. In contrast, the transient release of the anti-inflammatory cytokines IL-10 and IL-4 occurred later and was maximal at day 7. Both responses subsided by day 14. This early cytokine imbalance was associated with a brief rise in colonic and caecal histopathological injury score at day 7. The bacterial antigen-specific systemic response was found to follow the intestinal immune response with a maximal release of both pro- and anti-inflammatory cytokines at day 7. Thus, first exposure of healthy axenic wild-type mice to normal faecal flora and antigens results in an early proinflammatory cytokine response and transient colonic inflammation that then resolves in conjunction with a subsequent anti-inflammatory cytokine profile.

摘要

肠道微生物在慢性炎症性肠病的发生和持续中起着关键作用。在遗传易感宿主中,细菌定植导致快速发作的慢性肠道炎症。然而,对于在成熟免疫系统的断奶后动物的无菌肠道腔内,粪便细菌和抗原暴露所引起的肠道和全身免疫反应尚不清楚。本研究检查了粪便细菌和抗原暴露对健康无菌小鼠肠道黏膜和全身免疫系统的影响。无菌野生型小鼠经口接种来源于常规饲养小鼠的粗粪便悬浮液,并在处理前和处理后第 3、7、14 和 28 天进行分析。摄入粪便悬浮液导致短暂的、早期的促炎干扰素(IFN)-γ、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-17 反应,在第 3 天达到最大值。相比之下,抗炎细胞因子 IL-10 和 IL-4 的短暂释放发生得较晚,在第 7 天达到最大值。两种反应在第 14 天消退。这种早期细胞因子失衡与第 7 天结肠和盲肠组织病理学损伤评分的短暂升高有关。发现细菌抗原特异性全身反应跟随肠道免疫反应,在第 7 天释放最大量的促炎和抗炎细胞因子。因此,健康无菌野生型小鼠首次接触正常粪便菌群和抗原会导致早期促炎细胞因子反应和短暂的结肠炎症,随后伴随着抗炎细胞因子谱的出现而缓解。

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