來(lái)自天然腸道細(xì)菌的信號(hào)對(duì)于機(jī)體免疫效應(yīng)對(duì)抗病毒和細(xì)菌來(lái)說(shuō)非常有效,，這項(xiàng)研究成果由弗萊堡大學(xué)的研究者完成,，刊登在了近日的國(guó)際雜志Immunity上,。
數(shù)以萬(wàn)億計(jì)的細(xì)菌生存在健康人群以及其它動(dòng)物的腸道中，這種天然的腸道細(xì)菌對(duì)于維持機(jī)體消化和維生素代謝以及對(duì)于宿主的健康功不可沒(méi),。近日,，研究者通過(guò)研究指出腸道微生物菌群在腸道免疫系統(tǒng)的形成上扮演著重要作用，如果改變腸道菌群的組成將會(huì)增加食品過(guò)敏或者腸道炎性疾病的風(fēng)險(xiǎn),。以前我們并不清楚擴(kuò)大腸道菌群的廣度可以影響腸道外部的免疫過(guò)程,，比如抵御病毒的能力等等。
研究者用不同的過(guò)濾性病毒感染了兩組小鼠,，兩組小鼠中一組有正常的腸道菌群,，另外一組僅僅是所謂的無(wú)菌小鼠。相比正常小鼠來(lái)說(shuō),，無(wú)菌小鼠的免疫效應(yīng)會(huì)大幅降低,，并且產(chǎn)生嚴(yán)重的疾病，當(dāng)研究者給予無(wú)菌小鼠正常小鼠的體內(nèi)腸道微生物菌群時(shí),，其免疫效應(yīng)便可以恢復(fù),。
Diefenbach的研究小組在分子水平上成功地定位了無(wú)菌小鼠的缺陷，這些小鼠并不能產(chǎn)生可溶解的炎癥介質(zhì),，比如所謂的I型干擾素等,。來(lái)自天然免疫系統(tǒng)的樹(shù)突狀細(xì)胞可以通過(guò)產(chǎn)生介質(zhì)對(duì)感染快速應(yīng)答，如果其不存在的話(huà),，機(jī)體將不能針對(duì)細(xì)菌產(chǎn)生足夠的免疫防御力,，研究者揭示了來(lái)自腸道細(xì)菌的信號(hào)可以提供樹(shù)突狀細(xì)胞產(chǎn)生的條件，這種條件依賴(lài)于細(xì)胞核中DNA的水平,，并且使得基因編碼更多的可溶解性介質(zhì)來(lái)進(jìn)行識(shí)別,。研究者表示，這是首次揭示由于抗生素,、衛(wèi)生和生活方式的改變導(dǎo)致天然腸道菌群的改變,，進(jìn)而將影響機(jī)體整體的免疫系統(tǒng)。（生物谷Bioon.com）
編譯自：Natural Intestinal Flora Strengthen Immune System
doi:10.1016/j.immuni.2012.05.020
PMC:
PMID:
Priming of Natural Killer Cells by Nonmucosal Mononuclear Phagocytes Requires Instructive Signals from Commensal Microbiota
Stephanie C. Ganal Stephanie L. Sanos Carsten Kallfass Karin Oberle Caroline Johner Carsten Kirschning Stefan Lienenklaus Siegfried Weiss Peter Staeheli Peter Aichele Andreas Diefenbach
Mononuclear phagocytes are an important component of an innate immune system perceived as a system ready to react upon encounter of pathogens. Here, we show that in response to microbial stimulation, mononuclear phagocytes residing in nonmucosal lymphoid organs of germ-free mice failed to induce expression of a set of inflammatory response genes, including those encoding the various type I interferons (IFN-I). Consequently, NK cell priming and antiviral immunity were severely compromised. Whereas pattern recognition receptor signaling and nuclear translocation of the transcription factors NF-B and IRF3 were normal in mononuclear phagocytes of germ-free mice, binding to their respective cytokine promoters was impaired, which correlated with the absence of activating histone marks. Our data reveal a previously unrecognized role for postnatally colonizing microbiota in the introduction of chromatin level changes in the mononuclear phagocyte system, thereby poising expression of central inflammatory genes to initiate a powerful systemic immune response during viral infection.
