Pelaia Corrado, Pelaia Giulia, Maglio Angelantonio, Tinello Caterina, Gallelli Luca, Lombardo Nicola, Terracciano Rosa, Vatrella Alessandro
Department of Health Sciences, University "Magna Græcia" of Catanzaro, 88100 Catanzaro, Italy.
Department of Medicine, Surgery and Dentistry, University of Salerno, 84084 Salerno, Italy.
J Clin Med. 2023 May 9;12(10):3371. doi: 10.3390/jcm12103371.
Asthma and nasal polyposis often coexist and are frequently intertwined by tight pathogenic links, mainly consisting of the cellular and molecular pathways underpinning type 2 airway inflammation. The latter is characterized by a structural and functional impairment of the epithelial barrier, associated with the eosinophilic infiltration of both the lower and upper airways, which can be driven by either allergic or non-allergic mechanisms. Type 2 inflammatory changes are predominantly due to the biological actions exerted by interleukins 4 (IL-4), 13 (IL-13), and 5 (IL-5), produced by T helper 2 (Th2) lymphocytes and group 2 innate lymphoid cells (ILC2). In addition to the above cytokines, other proinflammatory mediators involved in the pathobiology of asthma and nasal polyposis include prostaglandin D and cysteinyl leukotrienes. Within this context of 'united airway diseases', nasal polyposis encompasses several nosological entities such as chronic rhinosinusitis with nasal polyps (CRSwNP) and aspirin-exacerbated respiratory disease (AERD). Because of the common pathogenic origins of asthma and nasal polyposis, it is not surprising that the more severe forms of both these disorders can be successfully treated by the same biologic drugs, targeting many molecular components (IgE, IL-5 and its receptor, IL-4/IL-13 receptors) of the type 2 inflammatory trait.
哮喘和鼻息肉常同时存在，且常因紧密的致病联系而相互交织，这些联系主要由支持2型气道炎症的细胞和分子途径组成。后者的特征是上皮屏障的结构和功能受损，伴有上下气道的嗜酸性粒细胞浸润，这可由过敏或非过敏机制驱动。2型炎症变化主要归因于辅助性T细胞2（Th2）淋巴细胞和2型固有淋巴细胞（ILC2）产生的白细胞介素4（IL-4）、13（IL-13）和5（IL-5）所发挥的生物学作用。除上述细胞因子外，参与哮喘和鼻息肉病理生物学的其他促炎介质还包括前列腺素D和半胱氨酰白三烯。在这种“联合气道疾病”的背景下，鼻息肉包括多种疾病实体，如伴鼻息肉的慢性鼻-鼻窦炎（CRSwNP）和阿司匹林加重的呼吸系统疾病（AERD）。由于哮喘和鼻息肉有共同的致病起源，因此不足为奇的是，这两种疾病的更严重形式可以通过相同的生物药物成功治疗，这些药物针对2型炎症特征的许多分子成分（IgE、IL-5及其受体、IL-4/IL-13受体）。
