Staphylococcus aureus and its IgE-inducing enterotoxins in asthma: current knowledge
Staphylococcus aureus and its IgE-inducing enterotoxins in asthma: current knowledge
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DOI：
10.1183/13993003.01592-2019
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发表时间：
2020-04-01
影响因子：
24.3
通讯作者：
Broeker, Barbara M.
中科院分区：
文献类型：
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作者：
Bachert, Claus;Humbert, Marc;Broeker, Barbara M.
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 表达模式大多是多克隆的，尽管总 IgE 增加，但特异性 IgE 较低或低于检测水平。在晚发严重哮喘患者中，血清中经常检测到葡萄球菌肠毒素特异性 IgE (SE-IgE)，并且与哮喘相关，严重哮喘的定义是住院、口服类固醇和肺功能下降。最近，SE-IgE 被证明甚至可以预测未来十年发展为严重哮喘并加重。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 A (SpA) 等）在不同水平上操纵气道粘膜免疫学。呼吸道上皮释放 IL-33，并通过其受体 ST2 激活先天淋巴样细胞 (ILC)，这些 ILC 和 T 辅助 (Th) 2 细胞释放 2 型细胞因子，肥大细胞脱粒，大量局部 B 细胞激活和 IgE 形成，最后吸引嗜酸性粒细胞，随后释放细胞外陷阱，加剧上皮损伤并促进 通过形成夏科-莱登晶体来维持疾病持续是金黄色葡萄球菌操纵粘膜免疫的最显着标志。总之，金黄色葡萄球菌声称在严重气道炎症的协调以及当前和未来疾病的严重程度中发挥着重要作用。在这篇综述中，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。
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.