美國科學家近日研究發(fā)現(xiàn),，暴露于普通胃部細菌的小鼠會免于形成I型糖尿病,，這表明有些種類的細菌可能有助于預防I型糖尿病,。這項發(fā)現(xiàn)還支持了所謂的“衛(wèi)生學假說”——發(fā)達國家的人缺乏接觸寄生蟲、細菌和病毒,，這會導致過敏,、哮喘及其它免疫系統(tǒng)疾病風險的增加。相關論文9月21日在線發(fā)表于《自然》（Nature）雜志上,。
過去十年來,，越來越多的證據(jù)表明，環(huán)境對于過分活躍的免疫反應的形成具有一定作用,。較不發(fā)達國家的人過敏發(fā)生率較低,，不過他們一旦移居到發(fā)達國家，發(fā)病率就會急劇增加,?？茖W家在實驗室中也觀察到了相同的現(xiàn)象——非肥胖性糖尿病（NOD）小鼠自然喂養(yǎng)條件下發(fā)病率各有不同,，取決于它們所處的環(huán)境,。
在最新的研究中，美國芝加哥大學的Alexander V. Chervonsky和同事發(fā)現(xiàn),，先天免疫不足的NOD小鼠在正常狀態(tài)下不會形成糖尿病,。當NOD小鼠被飼養(yǎng)在無菌環(huán)境中時，由于缺乏“友好”的腸道細菌,，它們患上了嚴重的糖尿?。欢斔鼈儽┞队谌祟惸c道常見的無害細菌時,，它們形成糖尿病的幾率明顯要低得多,。
論文第一作者、美國耶魯大學醫(yī)學院的Li Wen說：“理解腸道細菌怎樣作用于免疫系統(tǒng)從而影響糖尿病和其它自身免疫性疾病的發(fā)生極為重要,，它將使我們能夠設計出新的方法,，通過改變友好腸道細菌的平衡來標靶免疫系統(tǒng)，從而防御糖尿病,。”（生物谷Bioon.com）
生物谷推薦原始出處：
Nature，doi:10.1038/nature07336,，Li Wen,，Alexander V. Chervonsky
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
1 Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
2 Center for Genome Sciences, Washington University School of Medicine, St Louis, Missouri 63108, USA
3 Department of Pathology, University of Chicago, Chicago, Illinois 60637, USA
4 The Jackson Laboratory, Bar Harbor, Maine 04609, USA
5 Department of Cellular and Molecular Medicine, School of Medical Science, Bristol University, Bristol, BS8 1TD, UK
6 Diabetes Center at the University of California San Francisco, San Francisco, California 94143, USA
7 These authors contributed equally to this work.
8 Present address: Department of Microbiology, Cornell University, Ithaca, New York 14850, USA
Type 1 diabetes (T1D) is a debilitating autoimmune disease that results from T-cell-mediated destruction of insulin-producing b-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.
