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    近日，來自日本理化研究所的研究人員通過研究揭示了腸道細菌對機體免疫系統成熟的作用，相關研究刊登于國際著名雜志Nature上，該研究也為揭示丁酸可以作為治療炎性腸病比如克羅恩病的有效療法。
 

    丁酸是腸道細菌消化膳食纖維后的一種副產品，其可以扮演表觀遺傳開關的作用，來通過誘導腸道中調節T細胞的產生從而增強機體的免疫系統功能。

    此前研究揭示，患炎性腸病的病人機體中缺少產生丁酸的菌群而且其腸道中丁酸的水平較低；然而丁酸之所以可以抗炎性，因為其是結腸內壁細胞重要的能量來源，這項研究也是首次揭示了丁酸在產生調節性T淋巴細胞方面的角色。

    文章中，研究者Hiroshi Ohno等人通過對小鼠模型進行調查揭示了共生微生物可以有效增強機體中調節性T細胞的數量；而共生細菌產生的丁酸，其作為一種短鏈脂肪酸可以促進機體中調節性T細胞的分化，而且也可以調節和天然T細胞分化有關的基因的表達。

    研究者Hiroshi Ohno說道，當給患大腸炎小鼠模型的飲食中添加部分丁酸后，其機體中調節性的T細胞水平明顯上升了，而且其疾病癥狀也明顯有所改善。調節性T細胞對于調節機體過度的炎性反應以及自體免疫疾病非常重要，這項研究為研究者開發預防以及治療炎性腸病的療法提供了一定思路，當然丁酸療法也是一種天然安全的療法，其對病人的作用顯而易見。（生物谷Bioon.com）

    Commensal microbe-derived butyrate induces the differentiation of colonic regulatory T cells

    Yukihiro Furusawa, Yuuki Obata, Shinji Fukuda, Takaho A. Endo, Gaku Nakato, Daisuke Takahashi, Yumiko Nakanishi, Chikako Uetake, Keiko Kato, Tamotsu Kato, Masumi Takahashi, Noriko N. Fukuda, Shinnosuke Murakami, Eiji Miyauchi, Shingo Hino, Koji Atarashi, Satoshi Onawa, Yumiko Fujimura, Trevor Lockett, Julie M. Clarke, David L. Topping, Masaru Tomita, Shohei Hori, Osamu Ohara, Tatsuya Morita et al.

    Gut commensal microbes shape the mucosal immune system by regulating the differentiation and expansion of several types of T cell1, 2, 3, 4, 5. Clostridia, a dominant class of commensal microbe, can induce colonic regulatory T （Treg） cells, which have a central role in the suppression of inflammatory and allergic responses3. However, the molecular mechanisms by which commensal microbes induce colonic Treg cells have been unclear. Here we show that a large bowel microbial fermentation product, butyrate, induces the differentiation of colonic Treg cells in mice. A comparative NMR-based metabolome **ysis suggests that the luminal concentrations of short-chain fatty acids positively correlates with the number of Treg cells in the colon. Among short-chain fatty acids, butyrate induced the differentiation of Treg cells in vitro and in vivo, and ameliorated the development of colitis induced by adoptive transfer of CD4+ CD45RBhi T cells in Rag1?/? mice. Treatment of naive T cells under the Treg-cell-polarizing conditions with butyrate enhanced histone H3 acetylation in the promoter and conserved non-coding sequence regions of the Foxp3 locus, suggesting a possible mechanism for how microbial-derived butyrate regulates the differentiation of Treg cells. Our findings provide new insight into the mechanisms by which host–microbe interactions establish immunological homeostasis in the gut.