PDF(Pubmed)
Abstract：
Long-term inflammatory skin disease atopic dermatitis is characterized by dry skin, itching, and eczematous lesions. During inflammation skin barrier protein impairment promotes S. aureus colonisation in the inflamed skin, worsening AD patient\'s clinical condition. Proteomic analysis revealed the presence of several immune evasion proteins and virulence factors in S. aureus extracellular vesicles (EVs), suggesting a possible role for these proteins in the pathophysiology of atopic dermatitis. The objective of this study is to assess the efficacy of a wall fragment obtained from a patented strain of C. acnes DSM28251 (c40) and its combination with a mucopolysaccharide carrier (HAc40) in counteract the pathogenic potential of EVs produced by S. aureus ATCC 14458. Results obtained from in vitro studies on HaCaT keratinocyte cells showed that HAc40 and c40 treatment significantly altered the size and pathogenicity of S. aureus EVs. Specifically, EVs grew larger, potentially reducing their ability to interact with the target cells and decreasing cytotoxicity. Additionally, the overexpression of the tight junctions mRNA zona occludens 1 (ZO1) and claudin 1 (CLDN1) following EVs exposure was decreased by HAc40 and c40 treatment, indicating a protective effect on the epidermal barrier\'s function. These findings demonstrate how Hac40 and c40 may mitigate the harmful effects of S. aureus EVs. Further investigation is needed to elucidate the exact mechanisms underlying this interaction and explore the potential clinical utility of c40 and its mucopolysaccharide carrier conjugate HAc40 in managing atopic dermatitis.
摘要：
长期炎症性皮肤病特应性皮炎的特征是皮肤干燥，瘙痒,和湿疹性病变。在炎症期间，皮肤屏障蛋白受损促进金黄色葡萄球菌在发炎的皮肤中定植，AD患者的临床状况恶化。蛋白质组学分析显示金黄色葡萄球菌细胞外囊泡（EV）中存在几种免疫逃避蛋白和毒力因子，提示这些蛋白质在特应性皮炎的病理生理学中可能发挥作用。这项研究的目的是评估从痤疮梭菌DSM28251（c40）的专利菌株获得的壁片段及其与粘多糖载体（HAc40）的组合在抵消由金黄色葡萄球菌产生的EV的致病潜力中的功效。从对HaCaT角质形成细胞的体外研究获得的结果显示,HAc40和c40处理显著改变金黄色葡萄球菌EV的大小和致病性。具体来说,电动汽车越来越大，潜在地降低它们与靶细胞相互作用的能力并降低细胞毒性。此外,HAc40和C40治疗降低了电动汽车暴露后紧密连接mRNA的过度表达，表明对表皮屏障的功能有保护作用。这些发现证明了Hac40和c40如何减轻金黄色葡萄球菌的有害影响。需要进一步的研究来阐明这种相互作用的确切机制，并探索c40及其粘多糖载体缀合物HAc40在治疗特应性皮炎中的潜在临床效用。
