3月22日，國(guó)際著名雜志Science在線刊登了國(guó)外研究人員的最新研究成果“Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function,，”,，文章中，研究者表示,，早期接觸微生物可通過(guò)改變自然殺傷細(xì)胞T細(xì)胞的數(shù)量和功能而抑制炎癥,。
研究者的這些發(fā)現(xiàn)提供了“衛(wèi)生學(xué)假說(shuō)”的證據(jù)；該假說(shuō)提出,，在世界上許多地方出現(xiàn)的哮喘及其它炎癥性疾病發(fā)生率的增加可能是因?yàn)樵谏脑缙谂c微生物接觸減少有關(guān),。 然而，微生物究竟是如何防止這些疾病的發(fā)生仍然是一個(gè)謎,。 Torsten Olszak及其同事現(xiàn)在用小鼠展示,，細(xì)菌群落幫助調(diào)節(jié)了小鼠結(jié)腸和肺內(nèi)的叫做自然殺傷性細(xì)胞T細(xì)胞或NKT細(xì)胞的免疫細(xì)胞的數(shù)量和功能。
無(wú)菌小鼠在這些組織中有著較高數(shù)量的NKT細(xì)胞,，而這又伴隨了CXCL16表達(dá)的增加,，CXCL16是與炎癥相關(guān)的一種受體。 無(wú)菌小鼠更容易罹患化學(xué)誘導(dǎo)的結(jié)腸炎（結(jié)腸的炎癥）并對(duì)過(guò)敏性哮喘的誘發(fā)更為敏感,。 給這些無(wú)菌小鼠重新植入不同的菌群防止了結(jié)腸炎及對(duì)哮喘的敏感性,，并使NKT細(xì)胞計(jì)數(shù)維持在低水平，但這些只發(fā)生在小鼠剛出生時(shí)接觸過(guò)細(xì)菌的情況下,。 在成年時(shí)接觸微生物無(wú)法令疾病和炎癥逆轉(zhuǎn),。 這些結(jié)果表明,，及早接觸微生物對(duì)免疫系統(tǒng)的炎癥敏感性具有重要且持久的影響。（生物谷Bioon.com）
doi:10.1126/science.1219328
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Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function
Torsten Olszak1,*, Dingding An2,*, Sebastian Zeissig3, Miguel Pinilla Vera4, Julia Richter5, Andre Franke6, Jonathan N. Glickman7, Reiner Siebert5, Rebecca M. Baron4, Dennis L. Kasper2,†‡, Richard S. Blumberg1,†‡
Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that, in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma compared to specific pathogen-free (SPF) mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal—but not adult—GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.
