Search

Chromoblastomycosis (CBM) is a chronic subcutaneous mycosis, caused by several dimorphic, pigmented dematiaceous fungi. Patients with the disease are still considered a therapeutic challenge, mainly due to its recalcitrant nature. There is no "gold standard" treatment for this neglected mycosis, but rather there are several treatment options. Chemotherapy alternatives include 5-flucytosine, itraconazole, terbinafine, fluconazole, thiabendazole, ketoconazole and amphotericin B, although the healing of severe cases is still uncommon. However, several studies have reported the DNA vaccine to be promising in the treatment for fungal infections; this vaccine allows the host to restore depressed cellular immunity, minimizing the toxic effects from conventional antifungal therapies. This work was therefore carried out aiming to establish a suitable model for experimental CBM, suggesting also new therapies, including DNA-hsp65 vaccine. By analyzing the morphometrical and histopathological aspects and by quantifying the fungal burden, the results showed the establishment of a chronic, although transitory, experimental CBM model with lesions similar to those presented in humans. A treatment regimen using intralesional itraconazole or amphotericin B was effective in treating experimental CBM, as was a therapy using naked DNA-hsp65 vaccine. It has also been shown that chemotherapy associated with DNA-hsp65 vaccine is promising in the treatment for CBM.

Chromoblastomycosis is a chronic, suppurative and granulomatous mycosis whose main etiologic agent is the fungus Fonsecaea pedrosoi. The severity of chromoblastomycosis clinical manifestations correlates with the Th1 or Th2 immune response, and an efficient cellular immune response depends on the interaction between immune cells and the cell wall of the fungi, which is able to promote this activation. The objective of this study was to analyze the influence of cell wall fractions of Fonsecaea pedrosoi on the activation of peritoneal phagocytes obtained from mice. Our results revealed that after 4 h of inoculation with fungal cell wall components, there was a cell migration predominantly comprised of neutrophils followed, after 72 h, by migration of the macrophages. After 4 h, the F2 fraction caused increased production of nitric oxide in phagocytes, but this effect was not observed in the phagocytes after 72 h. The F1 fraction stimulated production of IL-12 in cells that migrated after 72 h, while the inactivated fungus and the F2 fraction led to production of IL-10. The F2 fraction decreased the rate of phagocytosis and increased the production of IL-10. Our results suggest that the F2 fraction and its components caused an important disruption of microbicidal mechanisms negatively modulating the immune response and favoring the persistence of the fungus.