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首页> 外文期刊>Infection and immunity >Hyaluronan Modulation Impacts Staphylococcus aureus Biofilm Infection
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Hyaluronan Modulation Impacts Staphylococcus aureus Biofilm Infection

机译：透明质酸调节影响金黄色葡萄球菌生物膜感染。

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Staphylococcus aureus is a leading cause of chronic biofilm infections. Hyaluronic acid (HA) is a large glycosaminoglycan abundant in mammalian tissues that has been shown to enhance biofilm formation in multiple Gram-positive pathogens. We observed that HA accumulated in an S. aureus biofilm infection using a murine implant-associated infection model and that HA levels increased in a mutant strain lacking hyaluronidase (HysA). S. aureus secretes HysA in order to cleave HA during infection. Through in vitro biofilm studies with HA, the hysA mutant was found to accumulate increased biofilm biomass compared to the wild type, and confocal microscopy showed that HA is incorporated into the biofilm matrix. Exogenous addition of purified HysA enzyme dispersed HA-containing biofilms, while catalytically inactive enzyme had no impact. Additionally, induction of hysA expression prevented biofilm formation and also dispersed an established biofilm in the presence of HA. These observations were corroborated in the implant model, where there was decreased dissemination from an hysA mutant biofilm infection compared to the S. aureus wild type. Histopathology demonstrated that infection with an hysA mutant caused significantly reduced distribution of tissue inflammation compared to wild-type infection. To extend these studies, the impact of HA and S. aureus HysA on biofilm-like aggregates found in joint infections was examined. We found that HA contributes to the formation of synovial fluid aggregates, and HysA can disrupt aggregate formation. Taken together, these studies demonstrate that HA is a relevant component of the S. aureus biofilm matrix and HysA is important for dissemination from a biofilm infection.
机译：金黄色葡萄球菌是慢性生物膜感染的主要原因。透明质酸（HA）是一种在哺乳动物组织中丰富的大糖胺聚糖，已被证明可以增强多种革兰氏阳性病原体的生物膜形成。我们观察到，HA在使用鼠类植入物相关感染模型的金黄色葡萄球菌生物膜感染中积累，并且HA水平在缺乏透明质酸酶（HysA）的突变菌株中增加。金黄色葡萄球菌分泌HysA，以便在感染期间切割HA。通过HA的体外生物膜研究，发现 hysA 突变体与野生型相比积累了增加的生物膜生物量，并且共聚焦显微镜检查表明HA已整合到生物膜基质中。外源添加纯化的HysA酶可分散含有HA的生物膜，而催化惰性的酶则没有影响。此外，诱导 hysA 表达可防止生物膜形成，并在存在HA的情况下分散已建立的生物膜。这些观察结果在植入模型中得到了证实，其中与金黄色葡萄球菌野生型相比， hysA 突变生物膜感染的传播减少。组织病理学表明，与野生型感染相比，用 hysA 突变体感染引起的组织炎症分布明显减少。为了扩展这些研究，研究了HA和金黄色葡萄球菌HysA对关节感染中发现的生物膜样聚集体的影响。我们发现HA有助于滑液聚集体的形成，而HysA可以破坏聚集体的形成。综上，这些研究表明，HA是金黄色葡萄球菌生物膜基质的相关成分，而HysA对于生物膜感染的传播很重要。

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