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目的：初步探讨下呼吸道细菌感染/ 定植对慢性阻塞性肺疾病(COPD)患者痰β- 防御素2（BD-2）表达水平的影响。方法：36 例戒烟COPD 患者和30 名不吸烟/ 戒烟对照人员纳入研究。在COPD 患者的急性加重期和稳定期分别采集自然痰进行普通细菌培养（简称痰培养），并行细胞分类计数和BD-2 浓度测定；采集对照人员诱导痰行细胞分类计数和BD-2 浓度测定以资对照。结果：COPD 患者急性加重期和稳定期痰培养阳性比例分别为30/36 和14/36。COPD 患者痰细胞总数和中性粒细胞比例、淋巴细胞比例高于对照组而巨噬细胞比例低于对照组；痰菌阳性和痰菌阴性的急性加重期COPD 患者痰细胞总数、巨噬细胞比例、中性粒细胞比例分别为（6.0±0.9）×106/g、（23.6±3.9）%、（66.0±5.9）%和（3.1±0.5）×106/g、（34.3±4.3）%、（55.7±4.4）% ，痰菌阳性和痰菌阴性的稳定期COPD 患者痰细胞总数、巨噬细胞比例、中性粒细胞比例、淋巴细胞比例分别为（4.4±0.8）×106/g、（28.6± 6.4）%、（64.0±7.2）%和（3.0±0.5）×106/g、（41.4±5.7）%、（45.4±5.1）%。COPD 患者稳定期痰BD-2 浓度[(211±98)ng/L] 低于急性加重期[(300±83)ng/L] 而高于对照组[(127±41)ng/L]；痰菌阳性稳定期COPD 患者痰BD-2 浓度高于对照组而与急性加重期无统计学差异；痰菌阴性稳定期COPD 患者痰BD-2 浓度低于急性加重期而与对照组无统计学差异。结论：下呼吸道细菌感染/ 定植是COPD 患者痰BD-2 表达升高的重要诱导因素,也是COPD 患者急性加重发作的重要原因。

英文摘要:

Objective: To preliminary investigate the effect of lower respiratory tract bacterial infection / colonization on sputum β-defensin 2 (BD-2) expressions in chronic obstructive pulmonary disease (COPD) patients. Methods: Thirty-six COPD patients and 30 control subjects have been enrolled for the study, the subjects staff were either never-smoker or ex-smoker. Natural sputum were collected from COPD patients in both exacerbation and stable phases, and submitted for ordinary bacterial culture (referred to as sputum culture), differential cell count, and BD-2 concentration measurement. As control, induced sputum were collected from control subjects, and presented for differential cell count as well as BD-2 concentration measurement. Results: The positive result proportion of sputum culture were 30/36 for exacerbation phase and 14/36 for stable phase. As regard to differential sputum cell count, compared with control, the sputum of COPD patients account for increased total cell amount, increased neutrophils proportion, increased lymphocyte proportion, and decreased macrophages proportion. The items of sputum total cells count, macrophages percentage, neutrophils percentage were (6.0 ±0.9)×106 g-1, (23.6±3.9) %, (66.0± 5.9) % , respectively, for sputum-positive acute exacerbation COPD patients, and (3.1 ± 0.5) × 106 g-1, (34.3 ± 4.3) %, ( 55.7 ± 4.4) % for sputum- negative acute exacerbation COPD patients, while, (4.4 ± 0.8) × 106 g-1, (28.6±6.4) %, (64.0 ± 7.2) % for sputum-positive stable COPD patients, nevertheless,（3.0±0.5）×106 g-1, (41.4±5.7) %, (45.4±5.1) % for sputum-negative stable COPD patients. The sputum BD-2 concentration of stable COPD patients [(211 ± 98) ng L-1] were lower than acute exacerbation [(300 ± 83) ng L-1], whereas, higher than control subjects [(127 ± 41) ng L-1]. The sputum BD-2 concentration of stable sputum-positive COPD patients was not statistic different from exacerbation, and was higher than control. The sputum BD-2 concentration of stable sputum-negative COPD patients was lower than exacerbation, and was not statistic different from control. Conclusion: Lower respiratory tract bacterial infection / colonization induce the sputum BD-2 expression in COPD patients, which are important risk factors for acute exacerbation of COPD.

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