Host defense function of the airway epithelium in health and disease: clinical background
Host defense function of the airway epithelium in health and disease: clinical background
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DOI：
10.1189/jlb.0703315
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发表时间：
2004-01-01
影响因子：
5.5
通讯作者：
Johnston, SL
中科院分区：
文献类型：
--
作者：
Message, SD;Johnston, SL
呼吸道感染极为常见，是全世界发病率和死亡率的主要原因。气道上皮细胞在宿主防御感染中起着重要作用，本文通过考虑呼吸道病毒感染来说明这一点。在哮喘或慢性阻塞性肺疾病患者中，呼吸道病毒是病情加重的常见诱因。鼻病毒（RV）是最常见的病毒类型。这种RV诱导的急性加重的免疫发病机制的知识仍然有限，但信息可从体外和体内研究，特别是人类志愿者的实验感染。RV在下呼吸道的上皮细胞（EC）内感染和复制。EC是RV感染的先天免疫应答的重要组成部分。病毒与宿主细胞胞内信号传导途径之间的相互作用导致潜在抗病毒机制的激活，包括I型干扰素和一氧化氮，并导致细胞因子和趋化因子[白细胞介素（IL）-1 β、IL-6、IL-8、IL-11、IL-16、肿瘤坏死因子α、粒细胞巨噬细胞集落刺激因子、生长调节癌基因-α、上皮细胞嗜酸性粒细胞活化蛋白-78，调节活化，正常T细胞表达和分泌，嗜酸性粒细胞趋化因子1/2，巨噬细胞炎性蛋白-1 α]，其影响随后诱导的先天性和特异性免疫应答。虽然这有利于从呼吸道清除病毒，但促炎介质的产生和。炎性细胞的募集导致一定程度的免疫病理学，并可能放大预先存在的气道炎症。进一步的研究将是必要的，以确定是否修改EC呼吸道病毒感染的反应将是有益的治疗。
Respiratory infection is extremely common and a major cause of morbidity and mortality worldwide. The airway epithelium has an important role in host defense against infection and this is illustrated in this review by considering infection by respiratory viruses. In patients with asthma or chronic obstructive pulmonary disease, respiratory viruses are a common trigger of exacerbations. Rhinoviruses (RV) are the most common virus type detected. Knowledge of the immunopathogenesis of such RV-induced exacerbations remains limited, but information is available from in vitro and from in vivo studies, especially of experimental infection in human volunteers. RV infects and replicates within epithelial cells (EC) of the lower respiratory tract. EC are an important component of the innate-immune response to RV infection. The interaction between virus and the intracellular signaling pathways of the host cell results in activation of potentially antiviral mechanisms, including type I interferons and nitric oxide, and in the production of cytokines and chemokines [interleukin (IL)-1beta, IL-6, IL-8, IL-11, IL-16, tumor necrosis factor alpha, granulocyte macrophage-colony stimulating factor, growth-regulated oncogene-alpha, epithelial neutrophil-activating protein-78, regulated on activation, normal T expressed and secreted, eotaxin 1/2, macrophage-inflammatory protein-1alpha], which influence the subsequent induced innate- and specific-immune response. Although this is benefic-id in facilitating clearance of virus from the respiratory tract, the generation of proinflammatory mediators and. the recruitment of inflammatory cells result in a degree of immunopathology and may amplify pre-existing airway inflammation. Further research will be necessary to determine whether modification of EC responses to respiratory virus infection will be of therapeutic benefit.