Despite accumulating evidence indicating that Blastocystis hominis is pathogenic and that cysteine proteases are involved in its pathogenesis, few researches discussed the protease activity of B. hominis genetic subtypes. Therefore, the present study aims to identify the underlying pathogenic role of the proteases of B. hominis subtype 3 at different molecular weights in correlation to gastrointestinal symptoms. Of 65 patients with various clinical presentations referred to our laboratory for stool examination, 26 (40%) were B. hominis positive by stool culture. Of 26 (group I) B. hominis patients, 18 (69.2%) were symptomatic (group IA) and 8(30.8%) were asymptomatic (group IB). Of 25 normal control group (group II), 5 (20%) were B. hominis positive. Subtype 3 was the only genotype recovered by polymerase chain reaction. Of 26 patients in group I, 19 (73.1%) were immunocompetent and 7 (26.9%) were immunocompromised. Protease activities of B. hominis subtype 3 were recognized at 32-kDa (46.2%), 39-kDa (7.7%), 120-kDa (38.5%), 140-kDa (11.5%), and 215-kDa (19.2%) bands in gelatin sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Proteases were recognized in 17 (94.4%) out of 18 symptomatic Blastocystis patients versus 2 (25.0%) out of 8 asymptomatic patients. Proteases at 32 kDa were reported in 61.1% of symptomatic versus 12.5% of asymptomatic patients. It was concluded that proteases of B. hominis genetic subtype 3, particularly those at 32 kDa, could be considered a virulence factor that is responsible for protein degradation and have a possible pathogenic role in host immune evasion.
Cell-based therapy is emerging as a promising therapeutic approach for a wide range of liver diseases. This study aimed to investigate the regenerative and antifibrotic therapeutic potential of bone marrow-derived mesenchymal stem cells (BM-MSCs) in an early and late experimental hepatic schistosomiasis model. BM-MSCs were isolated from 6-wk-old BALB/c donor male mice, then grown and propagated in culture until cell count was 5-8 × 10(6)/ml. MSCs were then separated and injected into Schistosoma mansoni -infected female BALB/c mice on their 6, 10, 14, and 18 wk post-infection. Mice were sacrificed on the fourth and eighth week after BM-MSCs transplantation in each group. Homing of BM-MSCs was confirmed by PCR detection of male Y-chromosome gene (sry) in the liver tissue of the recipient female mice. The regenerative and antifibrotic potential of BM-MSCs was assessed by histopathological examination, morphometric analysis, electron microscopy, and liver function tests. Schistosoma-infected mice, which were treated with BM-MSCs, showed a decrease in the granuloma size, percentage and density of the fibrotic area, formation of new hepatocytes, and improvement of the liver function tests. Immunohistochemical examination of alpha-smooth muscle actin revealed a significant decrease in the immunoreactive hepatic stellate cells in mice treated with MSCs. Early granulomas (acute infection) showed better response to MSC injection than did later granulomas (chronic infection). Dosing and timing of MSCs transplantation should undergo more investigations in long-term experiments before application to the clinical field. This study is the first to assess and compare the effect of MSCs treatment on early and late granulomas.
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