Staphylococcus aureus is a noteworthy pathogen in allergic diseases, as four staphylococcal exotoxins activate mast cells, a significant contributor to inflammation, in an IgE‐independent manner. Although the adhesion of mast cells is an essential process for their immune responses, only a small number of exotoxins have been reported to affect the process. Here, we demonstrated that staphylococcal superantigen‐like (SSL) 3, previously identified as a toll‐like receptor 2 agonist, induced the adhesion of murine bone marrow‐derived mast cells to culture substratum. SSL3‐induced adhesion was mediated by fibronectin in an Arg‐Gly‐Asp (RGD) sequence‐dependent manner, suggesting the integrins were involved in the process. Additionally, SSL3 was found to bind to an anti‐adhesive surface protein CD43. SSL3 induced the adhesion of HEK293 cells expressing exogenous CD43, suggesting that CD43 is the target molecule for adhesion induced by SSL3. Evaluation of SSL3‐derived mutants showed that the C‐terminal region (253–326), specifically T285 and H307, are necessary to induce adhesion. SSL3 augmented the IL‐13 production of mast cells in response to immunocomplex and SSL12. These findings reveal a novel function of SSL3, triggering cell adhesion and enhancing mast cell activation. This study would clarify the correlation between S. aureus and allergic diseases such as atopic dermatitis.

中文翻译：

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葡萄球菌超抗原样蛋白 3 通过与 CD43 结合触发小鼠肥大细胞粘附并增强肥大细胞活化

金黄色葡萄球菌是过敏性疾病中值得注意的病原体，因为四种葡萄球菌外毒素以不依赖于 IgE 的方式激活肥大细胞，而肥大细胞是炎症的重要促成因素。尽管肥大细胞的粘附是其免疫反应的重要过程，但据报道，只有少数外毒素会影响该过程。在这里，我们证明了葡萄球菌超抗原样 (SSL) 3（之前被鉴定为 Toll 样受体 2 激动剂）可诱导小鼠骨髓来源的肥大细胞粘附到培养基质。SSL3 诱导的粘附是由纤连蛋白以 Arg-Gly-Asp (RGD) 序列依赖性方式介导的，表明整合素参与了该过程。此外，还发现 SSL3 可以与抗粘附表面蛋白 CD43 结合。SSL3诱导表达外源CD43的HEK293细胞的粘附，表明CD43是SSL3诱导粘附的靶分子。对 SSL3 衍生突变体的评估表明，C 末端区域 (253-326)，特别是 T285 和 H307，对于诱导粘附是必需的。SSL3 增强了肥大细胞对免疫复合物和 SSL12 的反应，产生 IL-13。这些发现揭示了 SSL3 的新功能，即触发细胞粘附并增强肥大细胞活化。这项研究将澄清之间的相关性金黄色葡萄球菌以及过敏性疾病，例如特应性皮炎。