While immunoglobulin (Ig) E is a prominent biomarker for early-onset, its levels are often elevated in non-allergic late-onset asthma. However, the pattern of IgE expression in the latter is mostly polyclonal, with specific IgEs low or below detection level albeit with an increased total IgE. In late-onset severe asthma patients, specific IgE to Staphylococcal enterotoxins (se-IgE) can frequently be detected in serum, and has been associated with asthma, with severe asthma defined by hospitalisations, oral steroid use and decrease in lung function. Recently, se-IgE was demonstrated to even predict the development into severe asthma with exacerbations over the next decade. Staphylococcus aureus manipulates the airway mucosal immunology at various levels via its proteins, including superantigens, serine-protease-like proteins (Spls), or protein A (SpA) and possibly others. Release of IL-33 from respiratory epithelium and activation of innate lymphoid cells (ILCs) via its receptor ST2, type 2 cytokine release from those ILCs and T helper (Th) 2 cells, mast cell degranulation, massive local B-cell activation and IgE formation, and finally eosinophil attraction with consequent release of extracellular traps, adding to the epithelial damage and contributing to disease persistence via formation of Charcot–Leyden crystals are the most prominent hallmarks of the manipulation of the mucosal immunity by S. aureus. In summary, S. aureus claims a prominent role in the orchestration of severe airway inflammation and in current and future disease severity. In this review, we discuss current knowledge in this field and outline the needs for future research to fully understand the impact of S. aureus and its proteins on asthma. Late-onset non-atopic, often severe asthma is not well understood. There is increasing evidence that bacteria and their proteins, specifically S. aureus and its superantigens and serine protease-like proteins may represent the triggers we are looking for. http://bit.ly/386oP4G

中文翻译：

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金黄色葡萄球菌及其在哮喘中诱导 IgE 的肠毒素：现有知识

虽然免疫球蛋白 (Ig) E 是早发性哮喘的重要生物标志物，但其水平在非过敏性迟发性哮喘中通常会升高。然而，后者的 IgE 表达模式主要是多克隆的，尽管总 IgE 增加，但特异性 IgE 较低或低于检测水平。在迟发性重度哮喘患者中，血清中经常可以检测到针对葡萄球菌肠毒素 (se-IgE) 的特异性 IgE，并且与哮喘相关，重度哮喘定义为住院、口服类固醇使用和肺功能下降。最近，se-IgE 被证明甚至可以预测未来十年内恶化为严重哮喘的发展。金黄色葡萄球菌通过其蛋白质（包括超抗原、丝氨酸蛋白酶样蛋白 (Spls)、或蛋白质 A (SpA) 和其他可能的。从呼吸道上皮释放 IL-33 并通过其受体 ST2 激活先天淋巴细胞 (ILC)，从这些 ILC 和 T 辅助 (Th) 2 细胞释放 2 型细胞因子，肥大细胞脱颗粒，大量局部 B 细胞激活和 IgE形成，最后是嗜酸性粒细胞吸引，随后释放细胞外陷阱，增加上皮损伤并通过形成 Charcot-Leyden 晶体导致疾病持续存在，这是金黄色葡萄球菌操纵粘膜免疫的最突出标志。总之，金黄色葡萄球菌在严重气道炎症的协调以及当前和未来的疾病严重程度方面发挥着重要作用。在这次审查中，我们讨论了该领域的当前知识，并概述了未来研究的需求，以充分了解金黄色葡萄球菌及其蛋白质对哮喘的影响。迟发性非特应性哮喘通常是严重的哮喘，目前尚不清楚。越来越多的证据表明，细菌及其蛋白质，特别是金黄色葡萄球菌及其超抗原和丝氨酸蛋白酶样蛋白质，可能是我们正在寻找的诱因。http://bit.ly/386oP4G