ABSTRACT
Objective To investigate the pathogenicity of Pneumocystis and its association with the development of chronic obstructive pulmonary disease (COPD). Methods The rat model of Pneumocystis pneumonia (PCP) was induced by intraperitoneal injection with dexamethasone, which was confirmed by pathogenic detection. The pathologic changes of rat lung specimens were examined using conventional HE staining, and the expression of inflammatory cells were detected by flow cytometry in bron-choalveolar lavage fluid (BALF) and splenic tissues of the rat model of PCP. In addition, the serum levels of matrix metalloproteinase 8 (MMP-8) and MMP-9 were measured using enzyme-linked immunosorbent assay (ELISA). Results Fusion and atrophy of alveolar spaces and hyperplasia of lung tissue were seen in the lung specimens of the rat model of PCP, and foam-like alveolar exudates and infiltration of inflammation cells were observed in the alveolar space, while severe infections exhibited consolidation of lung, which was similar to pathological features of COPD. The counts of CD8+ T lymphocytes (t = −7.920 and −12.514, P < 0.01), macrophages (t = −7.651 and −14.590, P < 0.01) and granulocytes (t = −10.310 and −16.578, P < 0.01) significantly increased and the counts of CD4+ T lymphocytes (t = 6.427 and 18.579, P < 0.01) significantly reduced in the BALF and splenic specimens of the rats with PCP relative to those without PCP. In addition, higher serum MMP-8 (t = −8.689, P < 0.01) and MMP-9 levels (t = −7.041, P < 0.01) were measured in rats with PCP than in those without PCP. Conclusion Pneumocystis infection may be associated with the development and progression of COPD.
ABSTRACT
Objective To investigate the pathogenicity of Pneumocystis and its association with the development of chronic obstructive pulmonary disease (COPD). Methods The rat model of Pneumocystis pneumonia (PCP) was induced by intraperitoneal injection with dexamethasone, which was confirmed by pathogenic detection. The pathologic changes of rat lung specimens were examined using conventional HE staining, and the expression of inflammatory cells were detected by flow cytometry in bron-choalveolar lavage fluid (BALF) and splenic tissues of the rat model of PCP. In addition, the serum levels of matrix metalloproteinase 8 (MMP-8) and MMP-9 were measured using enzyme-linked immunosorbent assay (ELISA). Results Fusion and atrophy of alveolar spaces and hyperplasia of lung tissue were seen in the lung specimens of the rat model of PCP, and foam-like alveolar exudates and infiltration of inflammation cells were observed in the alveolar space, while severe infections exhibited consolidation of lung, which was similar to pathological features of COPD. The counts of CD8+ T lymphocytes (t = −7.920 and −12.514, P < 0.01), macrophages (t = −7.651 and −14.590, P < 0.01) and granulocytes (t = −10.310 and −16.578, P < 0.01) significantly increased and the counts of CD4+ T lymphocytes (t = 6.427 and 18.579, P < 0.01) significantly reduced in the BALF and splenic specimens of the rats with PCP relative to those without PCP. In addition, higher serum MMP-8 (t = −8.689, P < 0.01) and MMP-9 levels (t = −7.041, P < 0.01) were measured in rats with PCP than in those without PCP. Conclusion Pneumocystis infection may be associated with the development and progression of COPD.