Pseudallescheria/Scedosporium species are medically important fungi that are present in soil and human impacted areas and capable of causing a wide spectrum of diseases in humans. Although little is known about their pathogenesis, their growth process and infection routes are very similar to those of Aspergillus species, which grow as biofilms in invasive infections. All nine strains tested here displayed the ability to grow as biofilms in vitro and to produce a dense network of interconnected hyphae on both polystyrene and the surfaces of central venous catheters, but with different characteristics. Scedosporium boydii and S. aurantiacum clinical isolates were able to form biofilms faster than the corresponding environmental strains, as evidenced in kinetic assays for S. boydii and CLSM for S. aurantiacum. Biofilms formed by Pseudallescheria/Scedosporium species had significantly higher resistance to the class of antifungal azole than was observed in planktonic cells, indicating a protective role for this structure. In addition, the clinical S. aurantiacum isolate that formed the most robust biofilms was also more virulent in a larvae Galleria mellonella infection model, suggesting that the ability to form biofilms enhances virulence in Pseudallescheria/Scedosporium species.
Composition and biomass of an Antarctic megafauna community were studied during a discontinuous 12 months cycle (March-December 1999 and December 2000-March 2001 at two stations (12 and 25 m depth) in Admiralty Bay, King George Island, Antarctica. During this period iceberg impacts were monitored in order to analyse their role in structuring the community. Organic matter content of the sediment showed a seasonal cycle for both depths, with lower values during winter and higher in summer. Composition and biomass of the megafauna were comparable to those described in previous surveys for the maritime Antarctica. Interannual or summer/winter changes in the density or biomass of the megafauna community were not significant, although significant differences between depths occurred during the whole survey. The observed community composition can be the considered result of a continuous invasion from a deeper fauna, constrained at shallower waters by the effects of ice and storms.
This study aimed to investigate the effects of cyclosporine on the morphology, cell wall structure, and secretion characteristics of Cryptococcus neoformans. The minimum inhibitory concentration (MIC) of cyclosporine was found to be 2 µM (2.4 µg/mL) for the H99 strain. Yeast cells treated with cyclosporine at half the MIC showed altered morphology, including irregular shapes and elongated projections, without an effect on cell metabolism. Cyclosporine treatment resulted in an 18-fold increase in chitin and an 8-fold increase in lipid bodies, demonstrating changes in the fungal cell wall structure. Cyclosporine also reduced cell body and polysaccharide capsule diameters, with a significant reduction in urease secretion in C. neoformans cultures. Additionally, the study showed that cyclosporine increased the viscosity of secreted polysaccharides and reduced the electronegativity and conductance of cells. The findings suggest that cyclosporine has significant effects on C. neoformans morphology, cell wall structure, and secretion, which could have implications for the development of new antifungal agents.
Cryptococcus neoformans is a fungal pathogen that causes life-threatening infections in immunocompromised individuals, who often have some inflammatory condition and, therefore, end up using glucocorticoids, such as dexamethasone and methylprednisolone. Although the effects of this class of molecules during cryptococcosis have been investigated, their consequences for the biology of C. neoformans is less explored. Here, we studied the effects of dexamethasone and methylprednisolone on the metabolism and on the induction of virulence factors in C. neoformans. Our results showed that both glucocorticoids increased fungal cell proliferation and surface electronegativity but reduced capsule and secreted polysaccharide sizes, as well as capsule compaction, by decreasing the density of polysaccharide fibers. We also tested whether glucocorticoids could affect the fungal virulence in Galleria mellonella and mice. Although the survival rate of Galleria larvae increased, those from mice showed a tendency to decrease, with infected animals dying earlier after glucocorticoid treatments. The pathogenesis of spread of cryptococcosis and the interleukin secretion pattern were also assessed for lungs and brains of infected mice. While increases in the spread of the fungus to lungs were observed after treatment with glucocorticoids, a significant difference in brain was observed only for methylprednisolone, although a trend toward increasing was also observed for dexamethasone. Moreover, increases in both pulmonary and cerebral IL-10 production, reduction of IL-6 production but no changes in IL-4, IL-17, and INF-γ were also observed after glucocorticoid treatments. Finally, histopathological analysis confirmed the increase in number of fungal cells in lung and brain tissues of mice previously subjected to dexamethasone or methylprednisolone treatments. Together, our results provide compelling evidence for the effects of dexamethasone and methylprednisolone on the biology of C. neoformans and may have important implications for future clinical treatments, calling attention to the risks of using these glucocorticoids against cryptococcosis or in immunocompromised individuals.
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