研究人員發(fā)現(xiàn)，阻斷肺部里的一種免疫細(xì)胞蛋白質(zhì)LIGHT,，能預(yù)防哮喘模式小鼠的呼吸道重構(gòu),，新成果發(fā)表在4月在線(xiàn)出版的《自然—醫(yī)學(xué)》期刊上。這項(xiàng)研究顯現(xiàn),，以該通道為靶標(biāo)可預(yù)防與哮喘有關(guān)的呼吸道重構(gòu)所帶來(lái)的呼吸問(wèn)題,。
嚴(yán)重哮喘患者在其肺部有慢性未解決的炎癥，這種炎癥導(dǎo)致呼吸道重構(gòu),、纖維化,，肺功能被降低。盡管目前治療哮喘的方法能控制呼吸道炎癥,，但卻基本上不能影響呼吸道的重構(gòu),。
Michael Croft和同事發(fā)現(xiàn)，當(dāng)免疫細(xì)胞因暴露于屋塵螨而被激活時(shí),，蛋白質(zhì)LIGHT也被表達(dá)出來(lái),，并導(dǎo)致呼吸道重構(gòu)。通過(guò)基因和抗體調(diào)控阻斷LIGHT的表達(dá),，就能在暴露于過(guò)敏原時(shí)預(yù)防呼吸道重構(gòu)和肺功能的降低,。（生物谷Bioon.com）
生物谷推薦原文：
Nature Medicine DOI:10.1038/nm.2356
The tumor necrosis factor family member LIGHT is a target for asthmatic airway remodeling
Taylor A Doherty; Pejman Soroosh; Naseem Khorram; Satoshi Fukuyama; Peter Rosenthal; Jae Youn Cho; Paula S Norris; Heonsik Choi; Stefanie Scheu; Klaus Pfeffer; Bruce L Zuraw; Carl F Ware; David H Broide; Michael Croft
Individuals with chronic asthma show a progressive decline in lung function that is thought to be due to structural remodeling of the airways characterized by subepithelial fibrosis and smooth muscle hyperplasia. Here we show that the tumor necrosis factor (TNF) family member LIGHT is expressed on lung inflammatory cells after allergen exposure. Pharmacological inhibition of LIGHT using a fusion protein between the IgG Fc domain and lymphotoxin β receptor (LTβR) reduces lung fibrosis, smooth muscle hyperplasia and airway hyperresponsiveness in mouse models of chronic asthma, despite having little effect on airway eosinophilia. LIGHT-deficient mice also show a similar impairment in fibrosis and smooth muscle accumulation. Blockade of LIGHT suppresses expression of lung transforming growth factor-β (TGF-β) and interleukin-13 (IL-13), cytokines implicated in remodeling in humans, whereas exogenous administration of LIGHT to the airways induces fibrosis and smooth muscle hyperplasia, Thus, LIGHT may be targeted to prevent asthma-related airway remodeling.
