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Pathogenesis of severe asthma

机译：严重哮喘的发病机制

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Patients with severe asthma have asthma symptoms which are difficult to control, require high dosages of medication, and continue to experience persistent symptoms, asthma exacerbations or airflow obstruction. Epidemiological and clinical evidences point to the fact that severe asthma is not a single phenotype. Cluster analyses have identified subclasses of severe asthma using parameters such as patient characteristics, and cytokine profiles have also been useful in classifying moderate and severe asthma. The IL-4/IL-13 signalling pathway accounts for the symptoms experienced by a subset of severe asthmatics with allergen-associated symptoms and high serum immunoglobulin E (IgE) levels, and these patients are generally responsive to anti-IgE treatment. The IL-5/IL-33 signalling pathway is likely to play a key role in the disease pathogenesis of those who are resistant to high doses of inhaled corticosteroid but responsive to systemic corticosteroids and anti-IL5 therapy. The IL-17 signalling pathway is thought to contribute to 'neutrophilic asthma'. Although traditionally viewed as players in the defence mechanism against viral and intracellular bacterial infection, mounting evidence supports a role for Th1 cytokines such as IL-18 and IFN-γ in severe asthma pathogenesis. Furthermore, these cytokine signalling pathways interact to contribute to the spectrum of clinical pathological outcomes in severe asthma. To date, glucocorticoids are the most effective anti-asthma drugs available, yet severe asthma patients are typically resistant to the effects of glucocorticoids. Glucocorticoid receptor dysfunction and histone deacetylase activity reduction are likely to contribute to glucocorticoid resistance in severe asthma patients. This review discusses recent development in different cytokine signalling pathways, their interactions and steroid resistance, in the context of severe asthma pathogenesis.
机译：患有严重哮喘的患者具有难以控制的哮喘症状，需要高剂量的药物治疗，并且继续经历持续的症状，哮喘加重或气流阻塞。流行病学和临床证据表明，严重哮喘并非单一表型。聚类分析已使用参数（例如患者特征）确定了严重哮喘的亚类，并且细胞因子谱也可用于对中度和重度哮喘进行分类。 IL-4 / IL-13信号通路解释了具有过敏原相关症状和高血清免疫球蛋白E（IgE）水平的重度哮喘患者所经历的症状，这些患者通常对抗IgE治疗有反应。 IL-5 / IL-33信号通路可能在那些对大剂量吸入皮质类固醇耐药但对全身性皮质类固醇和抗IL5治疗有反应的患者的发病中起关键作用。 IL-17信号传导途径被认为是导致“嗜中性哮喘”的原因。尽管传统上被视为对抗病毒和细胞内细菌感染的防御机制的参与者，但越来越多的证据支持Th1细胞因子（如IL-18和IFN-γ）在严重哮喘发病中的作用。此外，这些细胞因子信号传导途径相互作用，有助于严重哮喘的临床病理结果。迄今为止，糖皮质激素是可获得的最有效的抗哮喘药，但是严重的哮喘患者通常对糖皮质激素的作用具有抵抗力。糖皮质激素受体功能异常和组蛋白脱乙酰基酶活性降低可能会导致严重哮喘患者的糖皮质激素抵抗。这篇综述讨论了在严重哮喘发病机制中不同细胞因子信号传导途径，它们的相互作用和类固醇抗性的最新进展。

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