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would be interesting to determine if the PGs that C. neoformans secrete, correlate with the amount of capsule, melanin and other virulence factors. On the other hand, it was demonstrated that virulent forms of various fungi are able to decrease secretion of IL-12 in macrophages and increase secretion of IL-10, in contrast to nonvirulent forms that readily activate macrophages to secrete vast amount of IL-12. In the former case, immune response to the fungus is not adequate. As the amount of PGs in various systems influences the reciprocal regulation of IL-12 and IL-10, it is possible that Cryptococcus-derived PGs, as well as immune cells-derived, could disturb the balance between these two cytokines and shift the Th response from protective Th1 toward Th2. Then this would compromise resolution of the infection. If PGs secreted by Cryptococcus could increase virulence factors of the fungus and at the same time inhibit the Th1 response, thus leading to unresolved infection, then this could implicate use of nonsteroid antiinflammatory drugs as the additional therapy in fungal infections. Similar mechanisms of PGs activity may be investigated in other fungal pathogens like Aspergillus and Malassezia. For long-term investigation we would like to evaluate the factors of virulence and PGs production of Malassezia as factors important in the host immunomodulatory response by comparing the number and type of inflammatory cells and mediators in skin biopsies from normal and lesional skin in patients with SD and AD and in normal skin from HI. The progress in understanding of immunomodulatory mechanisms may lead to understanding the commensalism/pathogenicity dualism of Malassezia spp. We plan to test the PGs production of fungy by indometacin inhibitory growth assay and ELISA test. We hope that those properties of medically important fungal strains isolated in our country may contribute to the better understanding of the epidemiology and pathogenesis of human infections.

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fungi, laboratory diagnosis, susceptibility testing, factors of virulence, prostaglandins

Received: 17/6/2003

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