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作 者:郑权[1] 田景伦 刘霞[1] 何书经 康定理 漆自立[2]
机构地区:[1]成都市温江区人民医院,四川成都611130 [2]四川省人民医院,四川成都610072
出 处:《标记免疫分析与临床》2008年第6期346-348,共3页Labeled Immunoassays and Clinical Medicine
摘 要:为了了解吸烟对慢性阻塞性肺病患者血清IL-1β和IL-1Ra的影响,为吸烟介导慢性阻塞性肺病系统性炎症反应的机制提供新的证据,将38例慢性阻塞性肺病患者分为吸烟组与非吸烟组,用酶联免疫吸附试验方法检测患者血清IL-1β、IL-1Ra和IL-1β/IL-1Ra比值,并比较在两组间的差异。结果显示两组之间血清IL-1β、IL-1Ra和IL-1β/IL-1Ra比值的差异均有统计学意义(P<0.05),吸烟组血清IL-1β和IL-1β/IL-1Ra比值明显高于非吸烟组,IL-1Ra明显低于非吸烟组。提示吸烟不但明显增强COPD患者血清炎症细胞因子IL-1β的分泌,而且,还显著抑制了COPD患者分泌IL-1β的抑制因子IL-1Ra,从而进一步加重其系统性炎症反应。To investigate the effects of cigarette smoke on serum IL-1β and IL-1Ra in patients with chronic obstructive pulmonary disease (COPD), and demonstrate the new mechanism that cigarette smoke induces systemic inflammatory response in COPD, 38 patients with COPD were divided into smoking and non-smoking group, and the serum IL-1β and IL-1Ra levels were detected by enzyme linked-immuno-sorbent assay. The results showed that the differences of serum IL-1β, IL-1Ra and IL- 1β to IL-1Ra ratio were statistically significant ( P 〈 0.05 ) between smoking and non-smoking group in patients with COPD. The serum IL-1β and IL-1β to IL-1Ra ratio were significantly higher in smoking patients than that in non-smoking patients, while IL-1Ra was significantly lower in smoking patients than that in non-smoking patients. These data suggest that cigarette smoke not only significantly enhance inflammatory cytokine IL-1β secretion, but also obviously inhibit the secretion of the IL-1β inhibitor IL-1Ra, thereby its systemic inflammatory response is further increased in COPD patients.
关 键 词:慢性阻塞性肺病 白介素-1Β 白介素-1受体拮抗剂 吸烟 酶联免疫吸附试验
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