中国哮喘联盟

金黄色葡萄球菌及在哮喘中其肠毒素诱导的IgE的研究进展

2020/05/14

   摘要
   虽然免疫球蛋白(Ig)E是早期发作的重要生物标志物,但在非过敏性晚期发作的哮喘中,其水平经常升高。但在后者中的IgE表达模式主要是多克隆的,尽管总IgE有所增加,但特异性IgE仍低或低于检测水平。在迟发的重症哮喘患者中,可以经常在血清中检测到针对葡萄球菌肠毒素的特异性IgE(se-IgE),并且与哮喘和与住院、口服类固醇的使用和肺功能的下降为特征的重症哮喘有关。最近,已证明se-IgE甚至可以预测在未来十年内进展为重症哮喘的急性加重。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质(Spls)或蛋白质A(SpA)以及其他可能的蛋白质)在不同水平上操纵气道粘膜免疫。从呼吸道上皮释放IL-33并通过其受体ST2激活先天淋巴样细胞(ILC),从那些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的形成,嗜酸性粒细胞的趋化并释放细胞外捕获网,增加上皮细胞的损伤以及通过形成金黄色葡萄球菌对黏膜免疫最突出的特征性的夏科雷登结晶促进疾病的持久性。总之,金黄色葡萄球菌在编排严重气道炎症以及当前和将来的疾病严重性方面起着重要作用。在这篇综述中,我们讨论了该领域的现有知识,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对哮喘的影响。
 
 
 (中日友好医院呼吸与危重症医学科 张清 摘译 林江涛 审校)
(Eur Respir J. 2020 Apr 3;55(4):1901592.doi: 10.1183/13993003.01592-2019.)
 
 
 
Staphylococcus aureus and Its IgE-inducing Enterotoxins in Asthma: Current Knowledge
 
Claus Bachert, Marc Humbert , Nicola A Hanania , Nan Zhang , Stephen Holgate , Roland Buhl , Barbara M Bröker 
 
Abstract
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.
 


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