Phage "delay" towards enhancing bacterial escape from biofilms: a more comprehensive way of viewing resistance to bacteriophages
Phage "delay" towards enhancing bacterial escape from biofilms: a more comprehensive way of viewing resistance to bacteriophages
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DOI：
10.3934/microbiol.2017.2.186
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发表时间：
2017-01-01
影响因子：
4.8
通讯作者：
Abedon, Stephen T.
中科院分区：
文献类型：
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作者：
Abedon, Stephen T.
在探索细菌对噬菌体的抗性时，重点通常放在那些完全阻止噬菌体复制的机制上。这种抗性可以通过噬菌体形成噬斑的能力的广泛降低来检测，即电镀效率的降低。机制包括限制性修饰系统、CRISPR/Cas系统和流产感染系统。或者，当感染某些细菌宿主时，噬菌体的“活力”可能会降低，也就是说，噬菌体表现出较小的爆发大小或延长的潜伏期，而不是完全失活。众所周知，大多数噬菌体很难感染代谢活性较低的细菌。细胞外聚合物例如生物膜基质材料也可以至少减缓噬菌体渗透到细菌表面。在这里，我建议这种“不太稳健”的噬菌体抵抗机制可以通过减缓细菌生物膜内的噬菌体繁殖来为细菌服务，也就是说，延迟噬菌体对多种细菌的影响，而不是完全阻止这种影响。因此，相关细菌，即距离受感染细菌相对较近的细菌，例如大约10+μm远的细菌，更有可能通过标准传播启动机制（包括生物膜表面侵蚀或播种扩散/中心空心）从生物膜中逃逸。也就是说，考虑到噬菌体感染的局部区域，只要噬菌体从与易感细菌接触的初始点开始的传播速率可以降低，那么细菌的存活率就可以提高，因为细菌隐喻地“逃逸”到更多无噬菌体的位置。延迟机制——在某种程度上，它们在噬菌体的靶向方面不太具体——共同代表了噬菌体抗性与彻底噬菌体杀死的更广泛的细菌策略，后者尤其需要对噬菌体存在进行特定的、进化的分子识别。在制定噬菌体介导的生物膜细菌生物控制方案时，例如在慢性细菌感染的噬菌体治疗期间，应考虑噬菌体延迟的可能性。
In exploring bacterial resistance to bacteriophages, emphasis typically is placed on those mechanisms which completely prevent phage replication. Such resistance can be detected as extensive reductions in phage ability to form plaques, that is, reduced efficiency of plating. Mechanisms include restriction-modification systems, CRISPR/Cas systems, and abortive infection systems. Alternatively, phages may be reduced in their "vigor" when infecting certain bacterial hosts, that is, with phages displaying smaller burst sizes or extended latent periods rather than being outright inactivated. It is well known, as well, that most phages poorly infect bacteria that are less metabolically active. Extracellular polymers such as biofilm matrix material also may at least slow phage penetration to bacterial surfaces. Here I suggest that such "less-robust" mechanisms of resistance to bacteriophages could serve bacteria by slowing phage propagation within bacterial biofilms, that is, delaying phage impact on multiple bacteria rather than necessarily outright preventing such impact. Related bacteria, ones that are relatively near to infected bacteria, e.g., roughly 10+ mu m away, consequently may be able to escape from biofilms with greater likelihood via standard dissemination-initiating mechanisms including erosion from biofilm surfaces or seeding dispersal/ central hollowing. That is, given localized areas of phage infection, so long as phage spread can be reduced in rate from initial points of contact with susceptible bacteria, then bacterial survival may be enhanced due to bacteria metaphorically "running away" to more phage-free locations. Delay mechanisms-to the extent that they are less specific in terms of what phages are targeted-collectively could represent broader bacterial strategies of phage resistance versus outright phage killing, the latter especially as require specific, evolved molecular recognition of phage presence. The potential for phage delay should be taken into account when developing protocols of phage-mediated biocontrol of biofilm bacteria, e.g., as during phage therapy of chronic bacterial infections.