Department of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan; Virus Research Center, Clinical Research Division, Sendai Medical Center, Sendai 983-8520, Japan; Department of Advanced Preventive Medicine for Infectious Disease, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
Department of Kampo and Integrative Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan; Department of Education and Support for Regional Medicine, Tohoku University Hospital, Sendai 980-8574, Japan.
Respir Investig. 2023 Mar;61(2):270-283. doi: 10.1016/j.resinv.2022.11.002. Epub 2022 Dec 19.
Respiratory viruses like rhinovirus, influenza virus, respiratory syncytial virus, and coronavirus cause several respiratory diseases, such as bronchitis, pneumonia, pulmonary fibrosis, and coronavirus disease 2019, and exacerbate bronchial asthma, chronic obstructive pulmonary disease, bronchiectasis, and diffuse panbronchiolitis. The production of inflammatory mediators and mucin and the accumulation of inflammatory cells have been reported in patients with viral infection-induced respiratory diseases. Interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α, granulocyte-macrophage colony-stimulating factor, and regulated on activation normal T-cell expressed and secreted are produced in the cells, including human airway and alveolar epithelial cells, partly through the activation of toll-like receptors, nuclear factor kappa B and p44/42 mitogen-activated protein kinase. These mediators are associated with the development of viral infection-induced respiratory diseases through the induction of inflammation and injury in the airway and lung, airway remodeling and hyperresponsiveness, and mucus secretion. Medications used to treat respiratory diseases, including corticosteroids, long-acting β-agonists, long-acting muscarinic antagonists, mucolytic agents, antiviral drugs for severe acute respiratory syndrome coronavirus 2 and influenza virus, macrolides, and Kampo medicines, reduce the production of viral infection-induced mediators, including cytokines and mucin, as determined in clinical, in vivo, or in vitro studies. These results suggest that the anti-inflammatory effects of these medications on viral infection-induced respiratory diseases may be associated with clinical benefits, such as improvements in symptoms, quality of life, and mortality rate, and can prevent hospitalization and the exacerbation of chronic obstructive pulmonary disease, bronchial asthma, bronchiectasis, and diffuse panbronchiolitis.
呼吸道病毒,如鼻病毒、流感病毒、呼吸道合胞病毒和冠状病毒,可引起多种呼吸道疾病,如支气管炎、肺炎、肺纤维化和 2019 年冠状病毒病,并可使支气管哮喘、慢性阻塞性肺疾病、支气管扩张和弥漫性泛细支气管炎恶化。据报道,病毒感染引起的呼吸道疾病患者会产生炎症介质和粘蛋白,并积累炎症细胞。白细胞介素(IL)-1β、IL-6、IL-8、肿瘤坏死因子-α、粒细胞-巨噬细胞集落刺激因子和调节激活正常 T 细胞表达和分泌的物质在包括人气道和肺泡上皮细胞在内的细胞中产生,部分通过激活 toll 样受体、核因子 κB 和 p44/42 丝裂原激活蛋白激酶。这些介质通过诱导气道和肺部的炎症和损伤、气道重塑和高反应性以及粘蛋白分泌,与病毒感染引起的呼吸道疾病的发展有关。用于治疗呼吸道疾病的药物,包括皮质类固醇、长效β-激动剂、长效毒蕈碱拮抗剂、粘液溶解剂、严重急性呼吸综合征冠状病毒 2 和流感病毒的抗病毒药物、大环内酯类药物和汉方药,可减少临床、体内或体外研究中确定的病毒感染诱导介质的产生,包括细胞因子和粘蛋白。这些结果表明,这些药物对病毒感染引起的呼吸道疾病的抗炎作用可能与临床益处相关,例如改善症状、生活质量和死亡率,并可预防住院和慢性阻塞性肺疾病、支气管哮喘、支气管扩张和弥漫性泛细支气管炎的恶化。