Autor: |
Mazo Fávero Gimenes V; Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Avenida Prof. Lineu Prestes, 580 Bloco 17, CEP 05508-900, São Paulo, Brazil., Da Glória de Souza M, Ferreira KS, Marques SG, Gonçalves AG, Vagner de Castro Lima Santos D, Pedroso e Silva Cde M, Almeida SR |
Jazyk: |
angličtina |
Zdroj: |
Microbes and infection [Microbes Infect] 2005 Apr; Vol. 7 (4), pp. 708-13. Date of Electronic Publication: 2005 Mar 21. |
DOI: |
10.1016/j.micinf.2005.01.006 |
Abstrakt: |
Chromoblastomycosis is a chronic, often debilitating, suppurative, granulomatus mycosis of the skin and subcutaneous tissues beginning after inoculation trauma. It occurs world-wide, but is more frequently observed in tropical countries such as Brazil. The disease is usually insidious, and the lesions increase slowly but progressively, not responding to the usual treatments and quite often reappearing. The host defense mechanism in chromoblastomycosis has not been extensively investigated. Some studies have focused on fungus-host interaction, showing a predominantly cellular immune response, with the activation of macrophages involved in fungus phagocytosis. Although phagocytosis did occur, death of fungal cells was rarely observed. The ability of Fonsecaea pedrosoi to produce secreted or cell wall-associated melanin-like components, protects against destruction by host immune cells in vitro. Until now, the T cell immune response in chromoblastomycosis is undefined. In the present work, it was shown that, in patients with the severe form of the disease, predominant production of IL-10 cytokine, low levels of IFN-gamma and inefficient T cell proliferation were induced. In contrast, in patients with a mild form of the disease, predominant production of IFN-gamma cytokine, low levels of IL-10 and efficient T cell proliferation were observed. |
Databáze: |
MEDLINE |
Externí odkaz: |
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