Increased apoptosis during the early phase of experimental paracoccidioidomycosis as a phenotypic marker of resistance.

作者: Maurício A. Verícimo , Karla Marcelino França , Andrea C.V. Arnholdt , Thereza L. Kipnis

DOI: 10.1016/J.MICINF.2006.08.012

关键词:

摘要: Abstract Paracoccidiodomycosis (PCM) is a systemic mycosis that presents wide spectrum of clinical manifestations caused by Paracoccidiodes brasiliensis. The experimental murine model has been used to approach the disease with susceptible and resistant mouse strains reproduce most main human immunological features. We investigated whether pattern apoptosis peritoneal cells from two polar mice after infection P. brasiliensis could be associated susceptibility or resistance this pathogen. Apoptosis A/J (resistant), cultured in presence absence LPS as stimuli, was observed early on first day infection. Cells infected strain BALB/c did not exhibit persistently at lesser degree than mice. induced due nitric oxide, since its blockage either vitro vivo revert it. Analysis additional susceptibilities PCM assured dissociation NO production apoptosis. Interestingly, IL-6 IL-10 were secreted high amounts, might involved shielding Furthermore, IFNγ−/− show while Wt controls presented levels similar those amounts IFNγ IL-1β. expression Fas increased both mice, whereas FasL decreased significantly modulated TNFRI KO These results suggest mechanism control engagement otherwise contribute phenotype some

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