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.