Nature：细菌为什么会与人共存？

佚名

生物谷报道：为什么哺乳动物身上会有大量共生细菌生存？这些细菌又是怎样到它们身上去的？微生物学家正在开始了解这些问题。但是，将有益细菌与有害细菌区分开来的是什么仍然不大清楚。2005年，研究表明，小肠菌Bacteroides fragilis对哺乳动物免疫系统有深远影响，这种影响归于一个分子，即荚膜“多糖体-A”（PSA）。现在，B. fragilis PSA被发现能够在一个涉及可产生T-细胞的白介素-10的过程中保护动物不患细菌性和化学性结肠炎。这表明，B. fragilis通过抑制小肠炎症反应来帮助维持人体健康，共生因子也许能为寻找新疗法提供一个途径。本期封面图片（Tom DiCesere, Sarkis Mazmanian & Dennis Kasper）所示为肌动蛋白niof菌及其在人小肠中的共生因子。这个领域的工作正在得到以确定人体微生物环境性质及确定它在健康与疾病中所起作用为目的的几大研究项目的推动，其中包括“人类微生物组项目”（Human Microbiome Project）。在News Features文章中，Asher Mullard（p. 578）对不同的研究方法进行了分析；Apoorva Mandavilli（p. 581）报告了在小肠移植后从头开始观察肠道被细菌占据的一个难得机会。

生物谷推荐英文原文：

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: sarkis@caltech.edu) or D.L.K. (Email: dennis_kasper@hms.harvard.edu).

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.