Ojanguren I, Quirce S, Bobolea I, Pérez de Llano L, Del Pozo V
Respiratory Department, Hospital Universitari Vall d'Hebron, Departament de Medicina, Universitat Autònoma de Barcelona (UAB), Barcelona, Spain.
Vall d'Hebron Institut de Recerca (VHIR), Barcelona, Spain.
J Investig Allergol Clin Immunol. 2025 Feb 18;35(1):1-11. doi: 10.18176/jiaci.1043. Epub 2024 Nov 28.
Asthma, a prevalent chronic respiratory disease, manifests in heterogeneous phenotypes and endotypes, necessitating bespoke therapeutic approaches. Asthma exacerbations are characterized by worsening of symptoms and decline in lung function and present substantial challenges despite advances in understanding and treatment. Viral respiratory infections, notably those caused by rhinovirus, serve as primary triggers, with allergic sensitization and environmental exposures increasing susceptibility. Deficient antiviral responses in asthmatic airway epithelial cells, particularly impaired interferon production, perpetuate inflammation and hyperresponsiveness, contributing to exacerbations. Additionally, genetic polymorphisms influence host responses and susceptibility. Recent studies underscore the association between specific inflammatory profiles, particularly eosinophil-mediated inflammation, and the frequency of exacerbations. Biologic therapies targeting inflammatory pathways show promise in reducing the frequency of exacerbations, thus underscoring the importance of understanding inflammatory phenotypes when selecting treatment. Notably, T2 inhibitors may modulate immune responses, potentially mitigating viral exacerbations. Characterizing exacerbations is crucial for optimizing therapeutic strategies. Evidence suggests a dissociation between baseline inflammatory profiles and exacerbation phenotypes, highlighting the need for individualized management. Phenotyping exacerbations using sputum analysis helps to identify predominant inflammatory patterns and thus inform treatment decisions. The varied responses to biologic therapies further emphasize the importance of phenotyping exacerbations in refining treatment algorithms. In conclusion, phenotyping asthma exacerbations provides valuable insights into underlying inflammatory mechanisms and enables personalized therapy. Understanding the complex interplay between viral triggers, inflammatory pathways, and responses to treatment is essential if we are to effectively manage severe asthma and reduce the burden of exacerbations. Further research into the mechanistic actions of biologic therapies in mitigating viral exacerbations is warranted to optimize asthma management strategies.
哮喘是一种常见的慢性呼吸道疾病,表现为异质性的表型和内型,需要定制化的治疗方法。哮喘急性发作的特征是症状恶化和肺功能下降,尽管在认识和治疗方面取得了进展,但仍面临重大挑战。病毒性呼吸道感染,尤其是由鼻病毒引起的感染,是主要诱因,过敏致敏和环境暴露会增加易感性。哮喘气道上皮细胞中的抗病毒反应不足,特别是干扰素产生受损,会使炎症和高反应性持续存在,导致急性发作。此外,基因多态性会影响宿主反应和易感性。最近的研究强调了特定炎症特征,特别是嗜酸性粒细胞介导的炎症与急性发作频率之间的关联。针对炎症途径的生物疗法在降低急性发作频率方面显示出前景,因此突出了在选择治疗方法时了解炎症表型的重要性。值得注意的是,2型炎症(T2)抑制剂可能会调节免疫反应,有可能减轻病毒引起的急性发作。对急性发作进行特征描述对于优化治疗策略至关重要。有证据表明,基线炎症特征与急性发作表型之间存在脱节,这凸显了个性化管理的必要性。使用痰液分析对急性发作进行表型分析有助于识别主要的炎症模式,从而为治疗决策提供依据。对生物疗法的不同反应进一步强调了对急性发作进行表型分析在完善治疗方案中的重要性。总之,对哮喘急性发作进行表型分析有助于深入了解潜在的炎症机制,并实现个性化治疗。如果我们要有效管理重度哮喘并减轻急性发作的负担,了解病毒诱因、炎症途径和治疗反应之间的复杂相互作用至关重要。有必要进一步研究生物疗法在减轻病毒引起的急性发作方面的作用机制,以优化哮喘管理策略。