Influenza enhances caspase-1 in bronchial epithelial cells from asthmatic volunteers and is associated with pathogenesis.
Influenza enhances caspase-1 in bronchial epithelial cells from asthmatic volunteers and is associated with pathogenesis.
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DOI：
10.1016/j.jaci.2012.07.013
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发表时间：
2012-10
影响因子：
14.2
通讯作者：
Jaspers, Ilona
中科院分区：
文献类型：
--
作者：
Bauer, Rebecca N.;Brighton, Luisa E.;Mueller, Loretta;Xiang, Zhidan;Rager, Julia E.;Fry, Rebecca C.;Peden, David B.;Jaspers, Ilona
The leading cause of asthma exacerbation is respiratory viral infection. Innate antiviral defense pathways are altered in the asthmatic epithelium, yet involvement of inflammasome signaling in virus-induced asthma exacerbation is not known. To compare influenza-induced activation of inflammasome and innate immune signaling in human bronchial epithelial cells from asthmatics and non-asthmatics and investigate the role of caspase-1 in epithelial cell antiviral defense. Differentiated primary human bronchial epithelial cells from asthmatics and non-asthmatics were infected with influenza A virus. An inflammasome-specific quantitative real-time polymerase chain reaction array was used to compare baseline and influenza-induced gene expression profiles. Cytokine secretion, innate immune gene expression, and viral replication were compared between human bronchial epithelial cells from asthmatics and non-asthmatics. Immunofluorescence microscopy was used to evaluate caspase-1 and PYCARD co-localization. Tracheal epithelial cells from caspase-1 deficient or wildtype mice were infected with influenza and assessed for antiviral gene expression and viral replication. Human bronchial epithelial cells from asthmatics had altered influenza-induced expression of inflammasome-related and innate immune signaling components, which correlated with enhanced production of interlukin-1β, interleukin-6, and tumor necrosis factor-α. Specifically, influenza-induced caspase-1 expression was enhanced and localization differed in human bronchial epithelial cells from asthmatics compared to non-asthmatics. Influenza-infected tracheal epithelial cells from caspase-1 deficient mice had reduced expression of antiviral genes and viral replication. Caspase-1 plays an important role in the airway epithelial cell response to influenza infection, which is enhanced in asthmatics and may contribute to the enhanced influenza related pathogenesis observed in vivo.
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影响因子：
29.7
作者：
Davis BK;Wen H;Ting JP
通讯作者：
Ting JP
DOI：
10.1038/nri2851
发表时间：
2010-10
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
通讯作者：
--
DOI：
10.4049/jimmunol.0802367
发表时间：
2009-03-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Bryan NB;Dorfleutner A;Rojanasakul Y;Stehlik C
通讯作者：
Stehlik C
影响因子：
8
作者：
通讯作者：
--
DOI：
10.1513/pats.200806-054rm
发表时间：
2009-05-01
期刊：
Proceedings of the American Thoracic Society
影响因子：
--
作者：
Janssen-Heininger, Yvonne M W;Poynter, Matthew E;van der Vliet, Albert
通讯作者：
van der Vliet, Albert