Alvarado Israel, Abel-Santos Ernesto
School of Life Sciences, University of Nevada, Las Vegas, 4505 Maryland Parkway, Las Vegas, NV 89154, USA.
Future Microbiol. 2014;9(1):13-6. doi: 10.2217/fmb.13.141.
Ng KM, Ferreyra JA, Higginbottom SK et al. Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens. Nature 502(7469), 96-99 (2013). The human gut microbiota is a complex system of commensal microorganisms required for normal host physiology. Disruption of this protective barrier by antibiotics creates opportunities for enteric pathogens to establish infections. Although the correlation between the use of antibiotics and enteric infections have been known for some time, the specific signals that allow enteric pathogens to recognize a susceptible host have not been determined. In a recent article, Ng et al. demonstrated that the expansion of both Salmonella typhimurium and Clostridium difficile infections is enhanced by the availability of host-specific sugars liberated from the intestinal mucus by commensal bacteria. These results show how antibiotic removal of specific species from the gut microbiome allows symbiotic functions to be hijacked by pathogenic species.
吴凯明、费雷拉·哈维尔、希金博特姆·斯凯等。微生物群释放的宿主糖类促进肠道病原体抗生素后扩张。《自然》502(7469)，96 - 99(2013年)。人类肠道微生物群是正常宿主生理所需的共生微生物复杂系统。抗生素破坏这种保护屏障为肠道病原体建立感染创造了机会。虽然抗生素使用与肠道感染之间的关联已为人所知一段时间，但使肠道病原体识别易感宿主的具体信号尚未确定。在最近一篇文章中，吴等人证明，共生细菌从肠道黏液中释放的宿主特异性糖类可促进鼠伤寒沙门氏菌和艰难梭菌感染的扩张。这些结果表明，从肠道微生物组中去除特定物种的抗生素如何使致病物种劫持共生功能。
