Department of Pulmonary and Critical Care Medicine, Stanford University School of Medicine, Stanford, California 94305-5236, USA.
Otolaryngol Head Neck Surg. 2011 Jun;144(6):982-7. doi: 10.1177/0194599811400367. Epub 2011 Apr 5.
To determine if statins induce anti-inflammatory effects in upper airway inflammation. Mediators of innate and adaptive immunity regulate airway inflammation. Release of these mediators involves enzymatic conversion of polyunsaturated fatty acids into biologically active mediators, which can be blocked by statins. Although upper airway inflammation and chronic sinusitis occur in millions of patients with asthma worldwide, the anti-inflammatory effects of statins in upper airway inflammation have not been previously studied.
Laboratory research.
Tertiary referral center.
Analysis of sinus tissues collected from patients with chronic rhinosinusitis revealed suppression of highly expressed inflammatory mediators in patients who were found to be on statins, suggesting that statins may induce anti-inflammatory effects. Therefore, the authors performed an in vitro study to determine if these anti-inflammatory effects were induced by statins. Cultured primary human airway epithelial cells were exposed to ambient air pollution particulates (PM) to trigger the inflammation, with and without statins, and the expression of inflammatory mediators was analyzed.
The authors found that expression of CCL5, CCL11, and IL13RA was suppressed in patients on statins. In vitro exposure to PM enhanced the expression of these mediators, while pretreatment with statins completely blocked these effects. Furthermore, the effects of statins were blocked by inhibition of the statin pathway using isopentenyl-5-pyrophosphate. Statins did not have any significant effect on the viability of normal cells.
Statins induce anti-inflammatory effects in human airway epithelial inflammation. Statins may play a role in the treatment and prevention of chronic rhinosinusitis and pulmonary exacerbation of obstructive airway diseases.
确定他汀类药物是否在上呼吸道炎症中产生抗炎作用。先天和适应性免疫的介质调节气道炎症。这些介质的释放涉及多不饱和脂肪酸转化为生物活性介质的酶促转化，他汀类药物可以阻断该转化。尽管全世界有数百 万哮喘患者出现上呼吸道炎症和慢性鼻窦炎，但他汀类药物在上呼吸道炎症中的抗炎作用尚未得到研究。
实验室研究。
三级转诊中心。
对患有慢性鼻-鼻窦炎的患者的鼻窦组织进行分析，结果表明，正在服用他汀类药物的患者体内高度表达的炎症介质受到抑制，这表明他汀类药物可能具有诱导抗炎作用。因此，作者进行了一项体外研究，以确定这些抗炎作用是否由他汀类药物诱导。培养原代人呼吸道上皮细胞，使其暴露于环境空气污染物（PM）以引发炎症，同时加入和不加入他汀类药物，并分析炎症介质的表达。
作者发现，服用他汀类药物的患者的 CCL5、CCL11 和 IL13RA 的表达受到抑制。体外暴露于 PM 增强了这些介质的表达，而他汀类药物预处理完全阻断了这些作用。此外，使用异戊烯基-5-焦磷酸抑制他汀类药物途径可阻断他汀类药物的作用。他汀类药物对正常细胞的活力没有任何显著影响。
他汀类药物在上呼吸道上皮炎症中诱导抗炎作用。他汀类药物可能在治疗和预防慢性鼻-鼻窦炎和阻塞性气道疾病的肺部恶化方面发挥作用。
