Staphylococcus aureus (S. aureus) is one of the most common pathogen causing septic arthritis. To colonize the joints and establish septic arthritis this bacterium needs to resist the host innate immune responses. Lysozyme secreted by neutrophils and macrophages is an important defense protein present in the joint synovial fluids. S. aureus is known to be resistant to lysozyme due to its peptidoglycan modification by O-acetylation of N-acetyl muramic acid. In this study we have investigated the role of O-acetylated peptidoglycan in septic arthritis. Using mouse models for both local and hematogenous S. aureus arthritis we compared the onset and progress of the disease induced by O-acetyl transferase mutant and the parenteral wild type SA113 strain. The disease progression was assessed by observing the clinical parameters including body weight, arthritis, and functionality of the affected limbs. Further X-ray and histopathological examinations were performed to monitor the synovitis and bone damage. In local S. aureus arthritis model, mice inoculated with the ΔoatA strain developed milder disease (in terms of knee swelling, motor and movement functionality) compared to mice inoculated with the wild type SA113 strain. X-ray and histopathological data revealed that ΔoatA infected mice knee joints had significantly lesser joint destruction, which was accompanied by reduced bacterial load in knee joints. Similarly, in hematogenous S. aureus arthritis model, ΔoatA mutant strain induced significantly less severe clinical septic arthritis compared to its parental strain, which is in accordance with radiological findings. Our data indicate that peptidoglycan O-acetylation plays an important role in S. aureus mediated septic arthritis.

中文翻译：

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细胞壁肽聚糖O-乙酰化对脓毒性关节炎中金黄色葡萄球菌发病机理的影响。

金黄色葡萄球菌（S. aureus）是引起败血性关节炎的最常见病原体之一。为了定居关节并建立败血性关节炎，该细菌需要抵抗宿主的先天免疫反应。中性粒细胞和巨噬细胞分泌的溶菌酶是关节滑液中存在的重要防御蛋白。已知金黄色葡萄球菌对溶菌酶具有抗性，这是因为其通过N-乙酰基尿酸的O-乙酰化对肽聚糖进行修饰。在这项研究中，我们研究了O-乙酰化肽聚糖在脓毒性关节炎中的作用。使用针对局部和血源性金黄色葡萄球菌关节炎的小鼠模型，我们比较了由O-乙酰基转移酶突变体和肠胃外野生型SA113菌株诱导的疾病的发作和进展。通过观察临床参数（包括体重，关节炎和患肢的功能。进行了进一步的X射线和组织病理学检查以监测滑膜炎和骨损伤。在局部金黄色葡萄球菌关节炎模型中，与接种野生型SA113菌株的小鼠相比，接种ΔoatA菌株的小鼠发生的疾病较轻（在膝关节肿胀，运动和运动功能方面）。X射线和组织病理学数据显示，受ΔoatA感染的小鼠膝关节的关节破坏明显较小，并伴有膝关节细菌负荷降低。类似地，在血源性金黄色葡萄球菌关节炎模型中，与亲本菌株相比，ΔoatA突变株诱导的严重临床败血症性关节炎的发生率明显低于其亲本株。