健康小鼠的改色組織,，圖中顯示共生細(xì)菌存在于這些組織中,，腸上皮細(xì)胞為綠色。(Credit: Gregory Sonnenberg, Ph.D.; David Artis, Ph.D., Perelman School of Medicine University of Pennsylvania; Science)
健康人的腸道內(nèi)存在100萬億各種有益的細(xì)菌,，而且這些細(xì)菌僅僅在腸道內(nèi)生存,，幫助腸道消化食物。腸道中的共生細(xì)菌對(duì)人體有益,，在許多慢性病如艾滋病,、肥胖等疾病和腸道共生細(xì)菌擴(kuò)散到血液以及其它邊緣組織有密切關(guān)系，這就會(huì)引發(fā)病人的慢性炎癥,。因此,，如果共生細(xì)菌在不該生長(zhǎng)的地方繁殖，人類機(jī)體就會(huì)出現(xiàn)病癥,。
來自賓夕法尼亞大學(xué)的研究者發(fā)現(xiàn)機(jī)體皮膚,、腸道以及肺部表面被免疫細(xì)胞僅僅保護(hù)著，并且免疫細(xì)胞可以保護(hù)機(jī)體免于暴露于病毒,、細(xì)菌以及寄生蟲中,。目前免疫細(xì)胞控制腸道及其它屏障表面的共生細(xì)菌的繁殖場(chǎng)所的機(jī)理尚不清楚。
研究者Gregory在健康小鼠腸道組織中發(fā)現(xiàn)了固有的免疫細(xì)胞-先天淋巴細(xì)胞（innate lymphoid cells），這種免疫細(xì)胞可以限制共生細(xì)菌的繁殖場(chǎng)所,；如果先天淋巴細(xì)胞在小鼠中缺失,，共生細(xì)菌將會(huì)轉(zhuǎn)移至周緣組織并且促發(fā)炎癥。相關(guān)研究成果刊登在了近日的國(guó)際雜志Science上,。
值得注意的是,，研究者在周緣組織（peripheral tissues）發(fā)現(xiàn)的共生細(xì)菌屬于產(chǎn)堿菌屬的家族成員，這就意味著免疫系統(tǒng)可以進(jìn)行高度選擇性的途徑來調(diào)節(jié)控制不同種群的腸道共生菌,。研究者Artis表示,，令科學(xué)家一直迷惑的是人類機(jī)體如何進(jìn)化以協(xié)調(diào)這些共生細(xì)菌并且使這些共生細(xì)菌處于特定的區(qū)域。
先天淋巴細(xì)胞在慢性病人中可能會(huì)被損害,，導(dǎo)致病人機(jī)體中產(chǎn)堿菌的散布以及病理學(xué)的炎癥,，這或?qū)⒊蔀槿祟惣膊〉囊粋€(gè)新靶點(diǎn)。研究者的研究揭示了以先天淋巴細(xì)胞的效應(yīng)為靶點(diǎn)或者直接以特殊的共生細(xì)菌群組為靶點(diǎn)將對(duì)于治療某些慢性炎癥疾病會(huì)有一定幫助,。相關(guān)研究由美國(guó)胃腸病協(xié)會(huì)支持贊助,。（生物谷Bioon.com）
編譯自：Gut Immune Cells Keep Beneficial Microbes in Their Place
編譯者：天使托
doi:10.1126/science.1222551
PMC:
PMID:
Innate Lymphoid Cells Promote Anatomical Containment of Lymphoid-Resident Commensal Bacteria
Gregory F. Sonnenberg1, Laurel A. Monticelli1, Theresa Alenghat1, Thomas C. Fung1, Natalie A. Hutnick2, Jun Kunisawa3,4, Naoko Shibata3,4, Stephanie Grunberg1, Rohini Sinha1, Adam M. Zahm5, Mélanie R. Tardif6, Taheri Sathaliyawala7, Masaru Kubota7, Donna L. Farber7, Ronald G. Collman8, Abraham Shaked9, Lynette A. Fouser10, David B. Weiner2, Philippe A. Tessier6, Joshua R. Friedman5, Hiroshi Kiyono3,4,11, Frederic D. Bushman1, Kyong-Mi Chang8,12, David Artis1,13,*
The mammalian intestinal tract is colonized by trillions of beneficial commensal bacteria that are anatomically restricted to specific niches. However, the mechanisms that regulate anatomical containment remain unclear. Here, we show that interleukin-22 (IL-22)–producing innate lymphoid cells (ILCs) are present in intestinal tissues of healthy mammals. Depletion of ILCs resulted in peripheral dissemination of commensal bacteria and systemic inflammation, which was prevented by administration of IL-22. Disseminating bacteria were identified as Alcaligenes species originating from host lymphoid tissues. Alcaligenes was sufficient to promote systemic inflammation after ILC depletion in mice, and Alcaligenes-specific systemic immune responses were associated with Crohn’s disease and progressive hepatitis C virus infection in patients. Collectively, these data indicate that ILCs regulate selective containment of lymphoid-resident bacteria to prevent systemic inflammation associated with chronic diseases.
