生物谷報道：為什么哺乳動物身上會有大量共生細菌生存,？這些細菌又是怎樣到它們身上去的,？微生物學家正在開始了解這些問題。但是,，將有益細菌與有害細菌區(qū)分開來的是什么仍然不大清楚,。2005年，研究表明,，小腸菌Bacteroides fragilis對哺乳動物免疫系統(tǒng)有深遠影響，這種影響歸于一個分子,，即莢膜“多糖體-A”（PSA）?，F(xiàn)在，B. fragilis PSA被發(fā)現(xiàn)能夠在一個涉及可產(chǎn)生T-細胞的白介素-10的過程中保護動物不患細菌性和化學性結腸炎,。這表明,，B. fragilis通過抑制小腸炎癥反應來幫助維持人體健康，共生因子也許能為尋找新療法提供一個途徑,。本期封面圖片（Tom DiCesere, Sarkis Mazmanian & Dennis Kasper）所示為肌動蛋白niof菌及其在人小腸中的共生因子,。這個領域的工作正在得到以確定人體微生物環(huán)境性質及確定它在健康與疾病中所起作用為目的的幾大研究項目的推動，其中包括“人類微生物組項目”（Human Microbiome Project）,。在News Features文章中,，Asher Mullard（p. 578）對不同的研究方法進行了分析；Apoorva Mandavilli（p. 581）報告了在小腸移植后從頭開始觀察腸道被細菌占據(jù)的一個難得機會,。
生物谷推薦英文原文：
Nature 453, 620-625 (29 May 2008) | doi:10.1038/nature07008; Received 7 February 2008; Accepted 18 April 2008
A microbial symbiosis factor prevents intestinal inflammatory disease
Sarkis K. Mazmanian1,4, June L. Round1,4 & Dennis L. Kasper2,3
Division of Biology, California Institute of Technology, Pasadena, California 91125, USA
Channing Laboratory, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
These authors contributed equally to this work.
Correspondence to: Sarkis K. Mazmanian1,4Dennis L. Kasper2,3 Correspondence and requests for materials should be addressed to S.K.M. (Email: [email protected]) or D.L.K. (Email: [email protected]).
Humans are colonized by multitudes of commensal organisms representing members of five of the six kingdoms of life; however, our gastrointestinal tract provides residence to both beneficial and potentially pathogenic microorganisms. Imbalances in the composition of the bacterial microbiota, known as dysbiosis, are postulated to be a major factor in human disorders such as inflammatory bowel disease. We report here that the prominent human symbiont Bacteroides fragilis protects animals from experimental colitis induced by Helicobacter hepaticus, a commensal bacterium with pathogenic potential. This beneficial activity requires a single microbial molecule (polysaccharide A, PSA). In animals harbouring B. fragilis not expressing PSA, H. hepaticus colonization leads to disease and pro-inflammatory cytokine production in colonic tissues. Purified PSA administered to animals is required to suppress pro-inflammatory interleukin-17 production by intestinal immune cells and also inhibits in vitro reactions in cell cultures. Furthermore, PSA protects from inflammatory disease through a functional requirement for interleukin-10-producing CD4+ T cells. These results show that molecules of the bacterial microbiota can mediate the critical balance between health and disease. Harnessing the immunomodulatory capacity of symbiosis factors such as PSA might potentially provide therapeutics for human inflammatory disorders on the basis of entirely novel biological principles.
