The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model.
The epithelial anion transporter pendrin is induced by allergy and rhinovirus infection, regulates airway surface liquid, and increases airway reactivity and inflammation in an asthma model.
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上皮阴离子转运蛋白是由过敏和鼻病毒感染诱导的，调节气道表面液体，并增加哮喘模型中气道反应性和炎症。
DOI：
10.4049/jimmunol.181.3.2203
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发表时间：
2008-08-01
影响因子：
4.4
通讯作者：
Erle, David J.
中科院分区：
文献类型：
--
作者：
Nakagami, Yasuhiro;Favoreto, Silvio, Jr.;Zhen, Guohua;Park, Sung-Woo;Nguyenvu, Louis T.;Kuperman, Douglas A.;Dolganov, Gregory M.;Huang, Xiaozhu;Boushey, Homer A.;Avila, Pedro C.;Erle, David J.
Asthma exacerbations can be triggered by viral infections or allergens. The Th2 cytokines IL-13 and IL-4 are produced during allergic responses and cause increases in airway epithelial cell mucus, electrolyte and water secretion into the airway surface liquid (ASL). Since ASL dehydration can cause airway inflammation and obstruction, ion transporters could play a role in pathogenesis of asthma exacerbations. We previously reported that expression of the epithelial cell anion transporter pendrin is markedly increased in response to IL-13. Here we show that pendrin plays a role in allergic airway disease and in regulation of ASL thickness. Pendrin-deficient mice had less allergen-induced airway hyperreactivity and inflammation than control mice although other aspects of the Th2 response were preserved. In cultures of IL-13-stimulated mouse tracheal epithelial cells, pendrin deficiency caused an increase in ASL thickness, suggesting that reductions in allergen-induced hyperreactivity and inflammation in pendrin-deficient mice result from improved ASL hydration. To determine whether pendrin might also play a role in virus-induced exacerbations of asthma, we measured pendrin mRNA expression in human subjects with naturally occurring common colds caused by rhinovirus and found a 4.9-fold-increase in mean expression during colds. Studies of cultured human bronchial epithelial cells indicated that this increase could be explained by the combined effects of rhinovirus and IFN-γ, a Th1 cytokine induced during virus infection. We conclude that pendrin regulates ASL thickness and may be an important contributor to asthma exacerbations induced by viral infections or allergens.
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影响因子：
4.4
作者：
Kuperman, DA;Huang, XZ;Erle, DJ
通讯作者：
Erle, DJ
DOI：
10.1152/ajplung.00311.2001
发表时间：
2002-02-01
影响因子：
4.9
作者：
Danahay, H;Atherton, H;Poll, CT
通讯作者：
Poll, CT
影响因子：
5.3
作者：
Chen, Chun;Huang, Xiaozhu;Sheppard, Dean
通讯作者：
Sheppard, Dean
影响因子：
7.3
作者：
Hirsh, Andrew J.;Molino, Bruce F.;Johnson, M. Ross
通讯作者：
Johnson, M. Ross
影响因子：
15.9
作者：
Jayaraman, S;Song, YL;Verkman, AS
通讯作者：
Verkman, AS