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.
ABSTRACT
Spargana were collected from human and frogs in Liaoning and Hubei Provinces, China. PCR amplification and direct sequencing of A cox1 fragment was PCR-amplified from genomic DNA extracted from 7 specimens (5 from humans and 2 from frogs). The cox1 fragment (390 bp) showed 97–100% similarity to the reference sequence of S. erinaceieuropaei and 88–89% to the reference sequence of S. decipiens. There were 1–12 bases different between these worms, but no obvious genetic variation (0–3.3%) to the references. There was little difference of cox1 gene between sparganum samples of humans and frogs (1–3%). This study is the first report on S. erinaceieuropaei spargana from humans in Liaoning and Hubei Provinces.