Contribution of bacterial outer membrane vesicles to innate bacterial defense.

Contribution of bacterial outer membrane vesicles to innate bacterial defense.
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DOI:
10.1186/1471-2180-11-258
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发表时间:
2011-12-01
期刊:
影响因子:
4.2
通讯作者:
Kuehn MJ
Kuehn MJ
中科院分区:
生物学3区
文献类型:
--
作者:
Manning AJ;Kuehn MJ

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外膜囊泡 (OMV) 由革兰氏阴性菌在整个生长过程中组成型产生,并在毒力、炎症和包膜应激反应中发挥作用。在这里,我们研究外膜囊泡形成作为一种细菌机制,可立即短期保护免受外膜作用的应激源的影响。使用抗菌肽和噬菌体来检查 OMV 保护的有效性。我们发现,大肠杆菌的超囊泡突变体在抗菌肽 (AMP)、多粘菌素 B 和粘菌素治疗下的存活率比野生型更好。在大肠杆菌培养物中补充纯化的外膜囊泡可提供针对 AMP 的实质性保护,并且 AMP 显着诱导囊泡形成。在用多粘菌素 B 攻击的人类病原体产肠毒素大肠杆菌 (ETEC) 中也观察到了囊泡介导的保护和诱导囊泡形成。当 ETEC 与低浓度囊泡一起孵育并同时进行多粘菌素 B 处理时,细菌存活率立即增加,并且培养物获得了对多粘菌素 B 的抗性。相比之下,高水平的囊泡也提供了即时保护,但阻止了 获得抵抗力。 T4 噬菌体和 OMV 的共孵育显示出快速、不可逆的结合。 T4 感染的效率因与 OMV 形成复合物而显着降低。这些数据揭示了 OMV 通过吸附抗菌肽和噬菌体来促进先天细菌防御的作用。鉴于对抗菌肽的反应增加了囊泡形成,以及 T4-OMV 复合物感染效率的降低,我们得出结论,OMV 的产生可能是中和针对革兰氏阴性菌外膜的环境因子的重要因素。
Outer membrane vesicles (OMVs) are constitutively produced by Gram-negative bacteria throughout growth and have proposed roles in virulence, inflammation, and the response to envelope stress. Here we investigate outer membrane vesiculation as a bacterial mechanism for immediate short-term protection against outer membrane acting stressors. Antimicrobial peptides as well as bacteriophage were used to examine the effectiveness of OMV protection. We found that a hyper-vesiculating mutant of Escherichia coli survived treatment by antimicrobial peptides (AMPs) polymyxin B and colistin better than the wild-type. Supplementation of E. coli cultures with purified outer membrane vesicles provided substantial protection against AMPs, and AMPs significantly induced vesiculation. Vesicle-mediated protection and induction of vesiculation were also observed for a human pathogen, enterotoxigenic E. coli (ETEC), challenged with polymyxin B. When ETEC with was incubated with low concentrations of vesicles concomitant with polymyxin B treatment, bacterial survival increased immediately, and the culture gained resistance to polymyxin B. By contrast, high levels of vesicles also provided immediate protection but prevented acquisition of resistance. Co-incubation of T4 bacteriophage and OMVs showed fast, irreversible binding. The efficiency of T4 infection was significantly reduced by the formation of complexes with the OMVs. These data reveal a role for OMVs in contributing to innate bacterial defense by adsorption of antimicrobial peptides and bacteriophage. Given the increase in vesiculation in response to the antimicrobial peptides, and loss in efficiency of infection with the T4-OMV complex, we conclude that OMV production may be an important factor in neutralizing environmental agents that target the outer membrane of Gram-negative bacteria.
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