Synovial Fluid-Induced Aggregation Occurs across Staphylococcus aureus Clinical Isolates and is Mechanistically Independent of Attached Biofilm Formation.
Synovial Fluid-Induced Aggregation Occurs across Staphylococcus aureus Clinical Isolates and is Mechanistically Independent of Attached Biofilm Formation.
复制标题
滑液诱导的聚集跨越金黄色葡萄球菌临床分离株，并且在机械上独立于附着的生物膜形成。
DOI：
10.1128/spectrum.00267-21
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发表时间：
2021-10-31
影响因子：
3.7
通讯作者：
Stoodley P
中科院分区：
文献类型：
--
作者：
Staats A;Burback PW;Eltobgy M;Parker DM;Amer AO;Wozniak DJ;Wang SH;Stevenson KB;Urish KL;Stoodley P
目前正在研究快速滑液诱导的金黄色葡萄球菌聚集作为建立假体周围关节感染（PJIs）的重要因素。聚集体形成的致病优势已在体外得到充分证明，包括对抗生素的耐受性和对宿主免疫防御的保护。本工作的目的是通过测定21个临床S.使用成像和流式细胞术从PJI或血流感染培养的金黄色葡萄球菌分离物。此外，通过使用常规结晶紫测定法测量附着的细菌生物量，我们评估了聚集表型和表面相关生物膜形成之间是否存在相关性。虽然所有分离株在暴露于牛滑液（BSF）和人血清（HS）后均被刺激聚集，但单个菌株之间的聚集程度差异很大。有趣的是，PJI分离物在BSF暴露后比从血流感染中分离的分离物聚集得更多。虽然我们能够在生长培养基中刺激所有分离株的生物膜形成，但补充滑液或人血清在24小时孵育期间抑制细菌表面附着。令人惊讶的是，滑液诱导的聚集的程度和表面相关的生物膜的量之间没有相关性，如通过没有宿主流体补充的常规生物膜测定所测量的。总之，我们的研究结果表明，滑液诱导的聚集似乎是广泛的S。金黄色葡萄球菌菌株和机械独立的生物膜形成。重要性髋关节和膝关节植入物的细菌感染是骨科手术的罕见但毁灭性的并发症。尽管广泛认识到与假体关节感染的发展相关的相当大的经济、身体和情感负担，但对滑膜关节中细菌的建立仍然知之甚少。已经表明，一旦暴露于关节中的粘性流体滑液，金黄色葡萄球菌立即迅速形成对抗生素和宿主免疫细胞清除具有抗性的聚集体。与聚集体形成相关的细菌毒力可能是建立人工关节感染的一个步骤，因此，它有可能成为有效的预防目标。我们希望这项工作有助于未来开发针对滑液诱导聚集的治疗方法，以更好地预防和治疗这些感染。
Rapid synovial fluid-induced aggregation of Staphylococcus aureus is currently being investigated as an important factor in the establishment of periprosthetic joint infections (PJIs). Pathogenic advantages of aggregate formation have been well documented in vitro, including recalcitrance to antibiotics and protection from host immune defenses. The objective of the present work was to determine the strain dependency of synovial fluid-induced aggregation by measuring the degree of aggregation of 21 clinical S. aureus isolates cultured from either PJI or bloodstream infections using imaging and flow cytometry. Furthermore, by measuring attached bacterial biomass using a conventional crystal violet assay, we assessed whether there is a correlation between the aggregative phenotype and surface-associated biofilm formation. While all of the isolates were stimulated to aggregate upon exposure to bovine synovial fluid (BSF) and human serum (HS), the extent of aggregation was highly variable between individual strains. Interestingly, the PJI isolates aggregated significantly more upon BSF exposure than those isolated from bloodstream infections. While we were able to stimulate biofilm formation with all of the isolates in growth medium, supplementation with either synovial fluid or human serum inhibited bacterial surface attachment over a 24 h incubation. Surprisingly, there was no correlation between the degree of synovial fluid-induced aggregation and quantity of surface-associated biofilm as measured by a conventional biofilm assay without host fluid supplementation. Taken together, our findings suggest that synovial fluid-induced aggregation appears to be widespread among S. aureus strains and mechanistically independent of biofilm formation. IMPORTANCE Bacterial infections of hip and knee implants are rare but devastating complications of orthopedic surgery. Despite a widespread appreciation of the considerable financial, physical, and emotional burden associated with the development of a prosthetic joint infection, the establishment of bacteria in the synovial joint remains poorly understood. It has been shown that immediately upon exposure to synovial fluid, the viscous fluid in the joint, Staphylococcus aureus rapidly forms aggregates which are resistant to antibiotics and host immune cell clearance. The bacterial virulence associated with aggregate formation is likely a step in the establishment of prosthetic joint infection, and as such, it has the potential to be a potent target of prevention. We hope that this work contributes to the future development of therapeutics targeting synovial fluid-induced aggregation to better prevent and treat these infections.