Killing of Paracoccidioides brasiliensis yeast cells by IFN-gamma and TNF-alpha activated murine peritoneal macrophages: evidence of H(2)O(2) and NO effector mechanisms
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Data
2008-07-01
Autores
Moreira, Ana Paula [UNESP]
Dias-Melicio, Luciane Alarcao [UNESP]
Peraçoli, Maria Terezinha Serrão [UNESP]
Calvi, Sueli Aparecida [UNESP]
Soares, Ângela Maria Victoriano de Campos [UNESP]
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Springer
Resumo
Paracoccidioidomycosis is a deep mycosis, endemic in Latin America, caused by Paracoccidioides brasiliensis. Macrophage activation by cytokines is the major effector mechanism against this fungus. This work aimed at a better understanding of the interaction between yeast cells-murine peritoneal macrophages and the cytokine signals required for the effective killing of high virulence yeast-form of P. brasiliensis. In addition, the killing effector mechanisms dependent on the generation of reactive oxygen or nitrogen intermediates were investigated. Cell preincubation with IFN-gamma or TNF-alpha, at adequate doses, resulted in effective yeast killing as demonstrated in short-term (4-h) assays. Both, IFN-gamma and TNF-alpha activation were associated with higher levels of H(2)O(2) and NO when compared to nonactivation. Treatment with catalase (CAT), a H(2)O(2) scavenger, and N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide synthase inhibitor, reverted the killing effect of activated cells. Taken together, these results suggest that both oxygen and L-arginine-nitric oxide pathways play a role in the killing of highly virulent P. brasiliensis.
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Paracoccidioidomycosis, murine macrophages, fungicidal activity, cytokines, NO, H(2)O(2)
Como citar
Mycopathologia. Dordrecht: Springer, v. 166, n. 1, p. 17-23, 2008.