主页 > 医药科学 >
【medical-news】小鼠模型有助揭示OSA上气道炎症原
揟hese results could explain the inflammation observed in the upper airway of OSA patients,?Ramon Farr?(University of Barcelona, Spain) and colleagues write in the European Respiratory Journal.
Data from patient studies so far on the causes of this inflammation are inconclusive because different confounding pro-inflammatory stimuli (such as hypoxia, metabolic syndrome, and obesity) may contribute to the upper airway changes described in OSA.
Farr?and team established a realistic and well-controlled rat model in order to investigate whether a collapse−reopening stimulus similar to that experienced by patients with OSA is able to trigger an inflammatory response in the upper airway tissue.
The researchers found that rats subjected to a periodic pattern of recurrent negative and positive pressures to induce the collapse and reopening of the airway for 5 hours exhibited marked overexpression of pro-inflammatory biomarkers. Macrophage inflammatory protein (MIP)-2, tumor necrosis factor-α, interleukin-1b, and p-selectin levels were 40-, 24-, 47-, and 7-fold greater than for controls, respectively, in the larynx tissue. Similar results were found in the soft palate tissue, the authors report.
揟he mechanical stress associated with recurrent intraluminal pressure swings, collapse, and reopening triggers an inflammatory process in the upper airway,?the authors write.
揂ccordingly, it is expected that the chronic application of this mechanical challenge can give rise to inflammatory cellular infiltration and tissue changes causing the structural and functional upper airway injuries observed in patients, contributing to the 憊icious circle?that characterizes the progression of obstructive sleep apnea.?br>
In an accompanying editorial, A Shwartz (Johns Hopkins Sleep Disorders Center, Baltimore, Maryland, USA) and colleagues commented that the authors 搊ffer a rodent upper airway model to overcome inherent limitations of human studies and elucidate underlying pharyngeal mechanisms of sleep apnoea pathogenesis.?br>
Eur Respir J 2008: Advance online publication 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 2008年7月30日——医学在线新闻：研究报道，在大鼠诱导反复气道塌陷和重新开放，模拟阻塞性睡眠呼吸暂停（OSA）患者，能促进早期局部炎症的发展。
Ramon Farr（西班牙巴塞罗那大学）和其同事在欧洲呼吸病杂志中称，这些结果能解释发生于OSA患者的上气道炎症。
目前参加研究病人中这些炎症的诱因尚未确定，因为多种促炎症刺激（如缺氧，代谢综合征，肥胖）均参与了OSA患者上气道的改变。
Farr及其研究团队通过构建质控良好的大鼠模型来证明是否塌陷再开放刺激能够促发上气道的炎症，这种刺激存在于OSA病人中。
研究人员发现在接受正负压力诱导的气道塌陷——开放模型大鼠中，促炎症因子表达显著增加。模型组喉组织的巨噬细胞炎症蛋白（MIP）2，肿瘤坏死因子α，白介素1b，P选择蛋白水平分别是对照组的40，24，47和7倍。作者还报道在软腭组织也有类似结果。
作者说，机械压力相关的管腔内压力反复波动，塌陷，再开放促发上气道炎症过程。
据此，慢性机械刺激能增加炎症细胞浸润和组织改变，引起类似OSA患者的上气道结构和功能损伤，导致恶性循环，这是OSA患者病情进展的显著特征。
在相关评论中，Shwartz（美国马里兰州巴尔的摩约翰霍普金斯睡眠疾病中心）和其同事评论说，作者通过啮齿类动物上气道模型克服了人类研究方面的限制，阐明了睡眠呼吸暂停喉部病变的可能机制。 Jul 30, 2008 - MedWire News: Recurrent upper airway collapse and reopening induced in rats, mimicking that experienced by obstructive sleep apnea (OSA) patients, triggers an early local inflammatory process, researchers report.
2008年7月30日——医学在线新闻：研究报道，在大鼠诱导反复气道塌陷和重新开放，模拟阻塞性睡眠呼吸暂停（OSA）患者，能促进早期局部炎症的发展。
揟hese results could explain the inflammation observed in the upper airway of OSA patients,?Ramon Farr?(University of Barcelona, Spain) and colleagues write in the European Respiratory Journal.
Ramon Farr（西班牙巴塞罗那大学）和其同事在欧洲呼吸病杂志中称，这些结果能解释发生于OSA患者的上气道炎症。
Data from patient studies so far on the causes of this inflammation are inconclusive because different confounding pro-inflammatory stimuli (such as hypoxia, metabolic syndrome, and obesity) may contribute to the upper airway changes described in OSA.
阅读本文的人还阅读：
作者:admin@医学,生命科学 2011-04-07 18:33
医学,生命科学网