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目的测定慢性阻塞性肺疾病(COPD)急性加重期和稳定期患者血清白细胞介素32(IL-32)水平,以探讨IL-32在COPD发病机制中的作用。方法 2010年10月至2011年5月收集120例COPD患者,急性加重期60例,稳定期60例。另选同期30例非吸烟健康受试者作为对照组。用ELISA法检测血清IL-32和IL-8、肿瘤坏死因子α(TNF-α)含量,同时测定肺功能(FEV1%pred、FEV1/FVC),并分析IL-32水平与IL-8、TNF-α和气流阻塞之间的相关性。应用SPSS 13.0软件进行统计学分析,多组数据间比较采用单因素方差分析,采用Pearson相关分析进行相关性检验。结果 COPD急性加重期组血清IL-32的含量[(174.56±88.15)ng/L]显著高于对照组[(59.41±20.98)ng/L]和COPD稳定期组[(89.40±33.84)ng/L](P均<0.01),COPD稳定期组血清IL-32含量显著高于健康对照组(P值<0.01);COPD急性加重期组、稳定期组血清IL-32水平与IL-8、TNF-α呈正相关(P均<0.01),与FEV1%pred、FEV1/FVC和PaO2呈负相关(P均<0.01);不同严重程度COPD患者血清IL-8、TNF-α和IL-32含量比较无统计学意义(P均>0.05)。结论 COPD患者血清IL-32水平升高,可能与IL-8、TNF-α等炎性因子有关。IL-32可能作为一种促炎因子参与COPD的炎症反应。
Objective To determine the level of serum interleukin-32 (IL-32) in patients with chronic obstructive pulmonary disease (COPD) in acute exacerbation and stable phases to investigate the role of IL-32 in the pathogenesis of COPD. Methods A total of 120 COPD patients were collected from October 2010 to May 2011, with 60 cases of acute exacerbation and 60 cases of stable exacerbation. Another 30 healthy non-smoking subjects were selected as the control group. Serum levels of IL-32 and IL-8, TNF-α and FEV1 / FVC were measured by ELISA. The levels of IL-8 and IL-8, TNF -a and airflow obstruction. SPSS 13.0 software was used for statistical analysis. One-way analysis of variance (ANOVA) and Pearson correlation analysis were used to test the correlation between groups. Results The serum level of IL-32 in COPD group [(174.56 ± 88.15) ng / L] was significantly higher than that in control group [(59.41 ± 20.98) ng / L and [89.40 ± 33.84] ng / (P <0.01). The level of IL-32 in stable COPD group was significantly higher than that in healthy control group (P <0.01) (P <0.01), but negatively correlated with FEV1% pred, FEV1 / FVC and PaO2 (all P <0.01). The levels of IL-8, TNF-α and IL-32 in patients with different severity of COPD There was no statistical significance (P> 0.05). Conclusion Serum levels of IL-32 in COPD patients may be related to inflammatory factors such as IL-8 and TNF-α. IL-32 may participate in inflammation of COPD as a proinflammatory cytokine.