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【medical-news】《自然》：“友好”细菌帮助抵御
过去十年来，越来越多的证据表明，环境对于过分活跃的免疫反应的形成具有一定作用。较不发达国家的人过敏发生率较低，不过他们一旦移居到发达国家，发病率就会急剧增加。科学家在实验室中也观察到了相同的现象——非肥胖性糖尿病（NOD）小鼠自然喂养条件下发病率各有不同，取决于它们所处的环境。
在最新的研究中，美国芝加哥大学的Alexander V. Chervonsky和同事发现，先天免疫不足的NOD小鼠在正常状态下不会形成糖尿病。当NOD小鼠被饲养在无菌环境中时，由于缺乏“友好”的肠道细菌，它们患上了严重的糖尿病；而当它们暴露于人类肠道常见的无害细菌时，它们形成糖尿病的几率明显要低得多。
论文第一作者、美国耶鲁大学医学院的Li Wen说：“理解肠道细菌怎样作用于免疫系统从而影响糖尿病和其它自身免疫性疾病的发生极为重要，它将使我们能够设计出新的方法，通过改变友好肠道细菌的平衡来标靶免疫系统，从而防御糖尿病。”（科学网 梅进/编译）
（《自然》（Nature），doi:10.1038/nature07336，Li Wen，Alexander V. Chervonsky）
Letter
Nature advance online publication 21 September 2008 | doi:10.1038/nature07336; Received 18 July 2008; Accepted 8 August 2008; Published online 21 September 2008
Innate immunity and intestinal microbiota in the development of Type 1 diabetes
Li Wen1,7, Ruth E. Ley2,7,8, Pavel Yu. Volchkov3,7, Peter B. Stranges3,4, Lia Avanesyan3,4, Austin C. Stonebraker4, Changyun Hu1, F. Susan Wong5, Gregory L. Szot6, Jeffrey A. Bluestone6, Jeffrey I. Gordon2 & Alexander V. Chervonsky3,4
Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
Center for Genome Sciences, Washington University School of Medicine, St Louis, Missouri 63108, USA
Department of Pathology, University of Chicago, Chicago, Illinois 60637, USA
The Jackson Laboratory, Bar Harbor, Maine 04609, USA
Department of Cellular and Molecular Medicine, School of Medical Science, Bristol University, Bristol, BS8 1TD, UK
Diabetes Center at the University of California San Francisco, San Francisco, California 94143, USA
These authors contributed equally to this work.
Present address: Department of Microbiology, Cornell University, Ithaca, New York 14850, USA.
Correspondence to: Alexander V. Chervonsky3,4 Correspondence and requests for materials should be addressed to A.V.C. (Email: achervon@bsd.uchicago.edu).
Top of pageType 1 diabetes (T1D) is a debilitating autoimmune disease that results from T-cell-mediated destruction of insulin-producing -cells. Its incidence has increased during the past several decades in developed countries1, 2, suggesting that changes in the environment (including the human microbial environment) may influence disease pathogenesis. The incidence of spontaneous T1D in non-obese diabetic (NOD) mice can be affected by the microbial environment in the animal housing facility3 or by exposure to microbial stimuli, such as injection with mycobacteria or various microbial products4, 5. Here we show that specific pathogen-free NOD mice lacking MyD88 protein (an adaptor for multiple innate immune receptors that recognize microbial stimuli) do not develop T1D. The effect is dependent on commensal microbes because germ-free MyD88-negative NOD mice develop robust diabetes, whereas colonization of these germ-free MyD88-negative NOD mice with a defined microbial consortium (representing bacterial phyla normally present in human gut) attenuates T1D. We also find that MyD88 deficiency changes the composition of the distal gut microbiota, and that exposure to the microbiota of specific pathogen-free MyD88-negative NOD donors attenuates T1D in germ-free NOD recipients. Together, these findings indicate that interaction of the intestinal microbes with the innate immune system is a critical epigenetic factor modifying T1D predisposition. We are looking forward to inventing new methods for curing diabetes .
More and more people in China who live in country are suffering from diabetes, but they cann't afford to the treatments. [标签:content1][标签:content2]
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作者:admin@医学,生命科学 2011-06-03 17:11
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