Abstract:

Objective     To determine the concentration and differences of SIgA in bronchoalveolar lavage fluid (BALF) in the rat model of chronic obstructive pulmonary disease（COPD）, diabetes mellitus （DM）and chronic obstructive pulmonary disease plus diabetes mellitus（COPD+DM）.  Methods    48 rats were divided into four groups： the normal group, the COPD group, the DM group, and the COPD+DM group. There were 12 rats in each group. Bred in the experimental environment for one week, the DM  model was established. One week later, the COPD model was established by cigarette inhalation and intratracheal LPS exposure. After the rats were sacrificed, pathological changes of the right lung were observed, and the left lung was lavaged to determine the concentration of SIgA in BALF by ELISA.  Results     ① Pathological changes of lung tissue： in the normal group, the structure of alveolus was normal and  no inflammatory cell infiltration was found. In the COPD group,  the bronchial epithelium was ablated, and the interstitialpulmonary and airway walls were infiltrated with inflammatory cells, and the ruptured and enlarged alveolus and bullaes were identified. In the DM group, there was inflammatory cell infiltration under the basement membrane and the lodging cilias of bronchial epithelium. In the COPD+DM group, the bronchial epithelium was  severely ablated, and the interstitial-pulmonary and airway walls were infiltrated with abundant inflammatory cells.The structure of the alveolus were destroyed and some formed into bullaes. ② Concentration of SIgA in BALF： Compared with the normal group, the concentration of SIgA in the COPD group decreased (P<0.01), but increased in the DM group and the COPD+DM group (P<0.01). Compared with the COPD group, the concentration of SIgA in the DM group and the COPD+DM group significantly increased (P<0.01). There was no difference in the concentration of SIgA between the DM group and the COPD+DM group (P>0.05).  Conclusion    SIgA plays a defensive role in pulmonary mucosal immunity. Compared with the normal group, the significant decrease of SIgA in the COPD group indicates that the pulmonary mucosal immunity declines in the COPD group. The increased concentration of SIgA in the DM and COPD+DM group may be attributed to the immune response of advanced glycosylation end products (AGEs) and the increased compensatory immunity to pathogenic microorganisms.

Key words: Pulmonary disease, Chronic obstructive； Diabetes mellitus； Models, Animal； Bronchoalveolar lavage fluid； Immunoglobulin A, Secretory； Rats, Wistar