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腾讯登录Cell Host & Micro：细菌和免疫系统之间的斗争可导致慢性疾病的发生
| 导读 | 近日，来自乔治亚州立大学的研究者通过研究发现，肠道中正常生存的细菌和免疫系统之间的“战斗”，如果被另外一种细菌所打断，可能引发两种慢性疾病。研究中研究者揭示，当“煽动”细菌完全被清除掉之后，这种“战斗”仍然可以继续进行，而且进一步会引发代谢综合征或者炎性肠疾病。相关研究成果刊登在了近日的国际杂志<em>Cell Host & Microbe</em>上。
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近日，来自乔治亚州立大学的研究者通过研究发现，肠道中正常生存的细菌和免疫系统之间的“战斗”，如果被另外一种细菌所打断，可能引发两种慢性疾病。研究中研究者揭示，当“煽动”细菌完全被清除掉之后，这种“战斗”仍然可以继续进行，而且进一步会引发代谢综合征或者炎性肠疾病。相关研究成果刊登在了近日的国际杂志<em>Cell Host & Microbe</em>上。
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该项研究的结果对于理解慢性疾病如代谢综合征和慢性肠疾病等非常重要，代谢综合征包含很多风险因子，包括肥胖等，而慢性肠疾病（IBD）包括局限性肠炎和溃疡性结肠炎，可引发痢疾、出血等。
据统计，每年美国有超过600，000人回患上不同类型的炎性肠疾病。细菌一般情况下生存于人类肠道之中，细菌在维持人类健康上扮演着重要作用，粘膜免疫系统需要很好管理细菌的环境来避免炎性疾病的发生。
编译自：<a title="" href="http://www.sciencedaily.com/releases/2012/08/120802141529.htm" target="_blank">Bacteria-Immune System 'Fight' Can Lead to Chronic Diseases, Study Suggests</a>
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<img src="http://www.bioon.com/biology/UploadFiles/201208/2012080321380205.jpg" alt="" width="113" height="149" border="0" />
<a title="" href="http://dx.doi.org/doi:10.1016/j.chom.2012.07.004" target="_blank">doi:10.1016/j.chom.2012.07.004</a>
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<br/><strong>Transient Inability to Manage Proteobacteria Promotes Chronic Gut Inflammation in TLR5-Deficient Mice</strong><br/>
Frederic A. Carvalho1, 2, 3, Omry Koren4, Julia K. Goodrich4, Malin E.V. Johansson5, Ilke Nalbantoglu6, Jesse D. Aitken1, Yueju Su1, Benoit Chassaing1, William A. Walters7, Antonio González8, Jose C. Clemente9, Tyler C. Cullender4, Nicolas Barnich11, Arlette Darfeuille-Michaud11, Matam Vijay-Kumar1, Rob Knight9, 10, Ruth E. Ley4, Andrew T. Gewirtz1, ,
Colitis results from breakdown of homeostasis between intestinal microbiota and the mucosal immune system, with both environmental and genetic influencing factors. Flagellin receptor TLR5-deficient mice (T5KO) display elevated intestinal proinflammatory gene expression and colitis with incomplete penetrance, providing a genetically sensitized system to study the contribution of microbiota to driving colitis. Both colitic and noncolitic T5KO exhibited transiently unstable microbiotas, with lasting differences in colitic T5KO, while their noncolitic siblings stabilized their microbiotas to resemble wild-type mice. Transient high levels of proteobacteria, especially enterobacteria species including E. coli, observed in close proximity to the gut epithelium were a striking feature of colitic microbiota. A Crohn’s disease-associated E. coli strain induced chronic colitis in T5KO, which persisted well after the exogenously introduced bacterial species had been eliminated. Thus, an innate immune deficiency can result in unstable gut microbiota associated with low-grade inflammation, and harboring proteobacteria can drive and/or instigate chronic colitis.
<br/>来源：生物探索
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<!--more-->
该项研究的结果对于理解慢性疾病如代谢综合征和慢性肠疾病等非常重要，代谢综合征包含很多风险因子，包括肥胖等，而慢性肠疾病（IBD）包括局限性肠炎和溃疡性结肠炎，可引发痢疾、出血等。
据统计，每年美国有超过600，000人回患上不同类型的炎性肠疾病。细菌一般情况下生存于人类肠道之中，细菌在维持人类健康上扮演着重要作用，粘膜免疫系统需要很好管理细菌的环境来避免炎性疾病的发生。
编译自：<a title="" href="http://www.sciencedaily.com/releases/2012/08/120802141529.htm" target="_blank">Bacteria-Immune System 'Fight' Can Lead to Chronic Diseases, Study Suggests</a>
<div id="ztload">
<div> </div>
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201208/2012080321380205.jpg" alt="" width="113" height="149" border="0" />
<a title="" href="http://dx.doi.org/doi:10.1016/j.chom.2012.07.004" target="_blank">doi:10.1016/j.chom.2012.07.004</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Transient Inability to Manage Proteobacteria Promotes Chronic Gut Inflammation in TLR5-Deficient Mice</strong><br/>
Frederic A. Carvalho1, 2, 3, Omry Koren4, Julia K. Goodrich4, Malin E.V. Johansson5, Ilke Nalbantoglu6, Jesse D. Aitken1, Yueju Su1, Benoit Chassaing1, William A. Walters7, Antonio González8, Jose C. Clemente9, Tyler C. Cullender4, Nicolas Barnich11, Arlette Darfeuille-Michaud11, Matam Vijay-Kumar1, Rob Knight9, 10, Ruth E. Ley4, Andrew T. Gewirtz1, ,
Colitis results from breakdown of homeostasis between intestinal microbiota and the mucosal immune system, with both environmental and genetic influencing factors. Flagellin receptor TLR5-deficient mice (T5KO) display elevated intestinal proinflammatory gene expression and colitis with incomplete penetrance, providing a genetically sensitized system to study the contribution of microbiota to driving colitis. Both colitic and noncolitic T5KO exhibited transiently unstable microbiotas, with lasting differences in colitic T5KO, while their noncolitic siblings stabilized their microbiotas to resemble wild-type mice. Transient high levels of proteobacteria, especially enterobacteria species including E. coli, observed in close proximity to the gut epithelium were a striking feature of colitic microbiota. A Crohn’s disease-associated E. coli strain induced chronic colitis in T5KO, which persisted well after the exogenously introduced bacterial species had been eliminated. Thus, an innate immune deficiency can result in unstable gut microbiota associated with low-grade inflammation, and harboring proteobacteria can drive and/or instigate chronic colitis.
<br/>来源：生物探索
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