肺炎衣原体感染与慢性阻塞性肺疾病关系的研究

目的　探讨肺炎衣原体感染在慢性阻塞性肺疾病 (COPD)发病中的作用。方法　实验分 2部分 ,(1)动物实验 :雄性Wistar大鼠 4 0只 ,分为A、B、C、D组 ,每组 10只 ,除D组外分别予香烟烟雾吸入和 (或 )经气管滴入肺炎衣原体菌液。 6周后测肺功能 ,行肺部病变病理评分及PCR检测肺部肺炎衣原体感染情况。 (2 )临床研究 :用PCR测COPD患者 (17例 )及健康对照者 (19例 )肺脏肺炎衣原体DNA ,同时测血清肺炎衣原体IgG及IgA抗体。结果　 (1)B组和C组大鼠肺组织肺炎衣原体DNAPCR阳性率分别为 88 9%和 80 0 %。B组大鼠肺组织病理改变主要为炎性细胞浸润及小气道平滑肌增生 ,病理及肺功能改变均较A组显著 ;C组主要病理改变为气道壁炎性细胞浸润及平滑肌增生较明显 ,与D组比较差异有显著性 ,肺功能与D组比较无明显差异。 (2 )COPD患者血清IgG抗体阳性率为 82 4 % ,IgA为 5 8 8% ,均明显高于健康对照者 (P值均 <0 0 5 ) ;PCR检测患者肺组织肺炎衣原体DNA均为阴性。结论　肺炎衣原体感染与COPD无直接关系 ,即单纯肺炎衣原体感染不能引起COPD的发病 ,但它可在吸烟所致病变的基础上加重COPD的病理改变及气流阻塞。

The relationship between chronic obstructive pulmonary disease and Chlamydiae pneumoniae infection

Objective To determine the possible association between Chlamydiae pneumoniae (Cpn) infection and chronic obstructive pulmonary disease (COPD). Methods This work comprised of two studies. The first was an animal study which involved 40 male Wistar rats. The animals were divided into 4 groups,10 rats in each group. They were treated with cigarette smoking alone (group A),cigarette smoking and Cpn inoculation (group B),and Cpn inoculation alone (group C),respectively,with a group D as the control. After 6 weeks ,Cpn DNA in the lung tissue was detected by PCR,and pulmonary function of the animals was measured. Lung pathological characteristics were scored . In the second study we used PCR to detect Cpn DNA in lung tissues from patients with COPD and control group,meanwhile Cpn IgG and IgA antibodies were also measured. Results The animal model of COPD was successfully replicated in most rats of group A (88.9%) and all of group B (100%). Group A was greater than group B in changes of pulmonary function,and higher in pulmonary pathological scores,predominantly in inflammatory cell infiltration and proliferation of small airway smooth muscle .There were no statistical differences between group C and group D in changes of pulmonary function. Pulmonary pathological scores were higher in group C than in group D,with statistical value,also predominantly in inflammatory cell infiltration and proliferation of small airway smooth muscle . The positive incidence of Cpn PCR were 88.9% and 80.0% in group A and C respectively. The positive rate of IgG and IgA were 82.4% and 58.8%,respectively. All pulmonary biopsy specimens of COPD and control group were negative. Conclusions There were no direct relationship between COPD with Cpn infection. Infection with Cpn cannot induce COPD simply. But it can exacerbated the air obstruction of COPD on the bases of pulmonary impairment by cigarette smoking.