Maldonado Rita F, Sá-Correia Isabel, Valvano Miguel A
Institute for Bioengineering and Biosciences, Department of Bioengineering, Instituto Superior Técnico, Universidade de Lisboa, Lisbon, Portugal.
Department of Microbiology and Immunology, University of Western Ontario, London, ON, Canada.
FEMS Microbiol Rev. 2016 Jul;40(4):480-93. doi: 10.1093/femsre/fuw007. Epub 2016 Apr 12.
The Gram-negative bacterial lipopolysaccharide (LPS) is a major component of the outer membrane that plays a key role in host-pathogen interactions with the innate immune system. During infection, bacteria are exposed to a host environment that is typically dominated by inflammatory cells and soluble factors, including antibiotics, which provide cues about regulation of gene expression. Bacterial adaptive changes including modulation of LPS synthesis and structure are a conserved theme in infections, irrespective of the type or bacteria or the site of infection. In general, these changes result in immune system evasion, persisting inflammation and increased antimicrobial resistance. Here, we review the modifications of LPS structure and biosynthetic pathways that occur upon adaptation of model opportunistic pathogens (Pseudomonas aeruginosa, Burkholderia cepacia complex bacteria, Helicobacter pylori and Salmonella enterica) to chronic infection in respiratory and gastrointestinal sites. We also discuss the molecular mechanisms of these variations and their role in the host-pathogen interaction.
革兰氏阴性菌脂多糖（LPS）是外膜的主要成分，在宿主与病原体和先天免疫系统的相互作用中起关键作用。在感染过程中，细菌暴露于通常由炎症细胞和可溶性因子主导的宿主环境中，这些因子包括抗生素，它们为基因表达调控提供线索。细菌的适应性变化，包括LPS合成和结构的调节，是感染中的一个保守主题，无论细菌类型或感染部位如何。一般来说，这些变化会导致免疫系统逃避、持续炎症和抗菌耐药性增加。在这里，我们综述了模型机会致病菌（铜绿假单胞菌、洋葱伯克霍尔德菌复合体细菌、幽门螺杆菌和肠炎沙门氏菌）适应呼吸道和胃肠道慢性感染时LPS结构和生物合成途径的修饰。我们还讨论了这些变异的分子机制及其在宿主-病原体相互作用中的作用。
