Incorporation of collagen into Pseudomonas aeruginosa and Staphylococcus aureus biofilms impedes phagocytosis by neutrophils.
Incorporation of collagen into Pseudomonas aeruginosa and Staphylococcus aureus biofilms impedes phagocytosis by neutrophils.
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胶原蛋白掺入铜绿假单胞菌和金黄色葡萄球菌生物膜会阻碍中性粒细胞的吞噬作用。
DOI：
10.1101/2023.10.25.564018
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Gordon,VernitaD
中科院分区：
文献类型：
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作者：
Zhou,Xuening;Wells,MarilynJ;Gordon,VernitaD
生物膜是包埋在胞外聚合物（EPS）基质中的微生物群落。基质组分可以由生物膜生物体产生，也可以来源于环境，然后掺入生物膜中。例如，我们最近已经表明，胶原蛋白，一种宿主产生的蛋白质，在许多不同的感染部位都很丰富，可以被吸收到生物膜基质中，改变生物膜力学。生物膜基质保护细菌免受免疫系统的清除，并且其中一些保护可能来自生物膜的机械特性。铜绿假单胞菌和金黄色葡萄球菌是常见的人类病原体，以在富含胶原的解剖部位形成生物膜感染而闻名。在这里，我们表明，I型胶原蛋白纳入铜绿假单胞菌和S。金黄色葡萄球菌生物膜显著阻碍人嗜中性粒细胞对生物膜细菌的吞噬作用。然而，用胶原酶进行酶处理，可以分解胶原蛋白，可以部分或完全否定胶原蛋白的保护作用，并恢复中性粒细胞吞噬生物膜细菌的能力。从这些发现中，我们认为宿主材料的酶促降解可能是一种潜在的方式，可以在不促进抗生素耐药性的情况下损害生物膜感染并增强宿主免疫反应的功效。这种方法在感染物种已知的情况下以及在生物膜组分不容易已知的情况下（例如多物种感染或未知物种的感染）都可能是有益的。
Biofilms are communities of microbes embedded in a matrix of extracellular polymeric substances (EPS). Matrix components can be produced by biofilm organisms and can also originate from the environment and then be incorporated into the biofilm. For example, we have recently shown that collagen, a host-produced protein that is abundant in many different infection sites, can be taken up into the biofilm matrix, altering biofilm mechanics. The biofilm matrix protects bacteria from clearance by the immune system, and some of that protection likely arises from the mechanical properties of the biofilm. Pseudomonas aeruginosa and Staphylococcus aureus are common human pathogens notable for forming biofilm infections in anatomical sites rich in collagen. Here, we show that the incorporation of Type I collagen into P. aeruginosa and S. aureus biofilms significantly hinders phagocytosis of biofilm bacteria by human neutrophils. However, enzymatic treatment with collagenase, which breaks down collagen, can partly or entirely negate the protective effect of collagen and restore the ability of neutrophils to engulf biofilm bacteria. From these findings, we suggest that enzymatic degradation of host materials may be a potential way to compromise biofilm infections and enhance the efficacy of the host immune response without promoting antibiotic resistance. Such an approach might be beneficial both in cases where the infecting species is known and also in cases wherein biofilm components are not readily known, such as multispecies infections or infections by unknown species.