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Master's Dissertation
DOI
10.11606/D.9.2003.tde-21052009-094918
Document
Author
Full name
Karen Spadari Ferreira
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2003
Supervisor
Committee
Almeida, Sandro Rogério de (President)
Moreira, Adriana Pardini Vicentini
Vaz, Adelaide José
Title in Portuguese
Modulação da ativação de células dentríticas por Paracoccidioides brasiliensis
Keywords in Portuguese
Paracoccidioides brasiliensis (Estudo clínico)
Células dentríticas
gp43
Microbiologia médica
Paracoccidioidomicose
Abstract in Portuguese
A paracoccidioidomicose (PCM) é uma micose sistêmica, endêmica na América Latina, causada pelo fungo dimórfico térmico Paracoccidioides brasiliensis (P. brasiliensis), cujo principal componente antigênico é a glicoproteína de 43 kDa (gp43). Diferentes formas clínicas podem ser desenvolvidas e estão diretamente associadas com vários graus de depressão da resposta imune celular. Considerando a importância das células dendríticas na interação dos sistemas imune inato e adaptativo, e na ativação de células T "naive", no presente trabalho estudamos se células dendríticas interagem com leveduras de P. brasiliensis, assim como seu principal componente antigênico (gp43). Foi demonstrado pela primeira vez que células dendríticas poderiam ser infectadas por leveduras de P. brasiliensis, e esse fungo permaneceu viável após fagocitose. Analisamos por citometria de fluxo a expressão das moléculas de superfície observando diminuição significativa da expressão das moléculas de MHC-II, CD80 e CD54 em células dendríticas quando estas foram incubadas com leveduras da cepa Pb18 ou com gp43. Esse resultado mostrou que a ação do P. brasiliensis em células dendríticas poderia ser mediada pela gp43. Ao analisarmos a síntese de IL-12, observamos diminuição significativa desta interleucina, quando células dendríticas ativadas com LPS, foram cultivadas na presença de leveduras de P. brasiliensis ou gp43. Esses resultados sugerem que a gp43 pode afetar várias funções das células hospedeiras, indicando que esta inibição pode ser usada pelo P. brasiliensis para reduzir a eficiência da resposta imune, facilitando assim o estabelecimento da infecção primária indivíduos suscetíveis.
Title in English
Modulation, activation of Dentritic cells by Paracoccidioides brasiliensis
Keywords in English
Paracoccidioides brasiliensis
Dendritic cells
gp43
Medical microbiology
Paracoccidioidomycosis
Abstract in English
Paracoccidioidomycosis, endemic in Latin America, is a progressive systemic mycosis caused by dimorphic fungus Paracoccidioides brasiliensis, where the major antigenic component is a glycoprotein of 43kDa (gp43). The infection can evolve to different clinical forms that are associated to various degrees of suppressed cell-mediated immunity. The role of dendritic cells (DCs) in P.brasiliensis infection has never been investigated. With the recognition that DCs are able to initiate response in naïve T cells and that they also participate in Th cell education the present study was undertaken to understand whether DCs interact with P. brasiliensis or gp43, as well as to elucidate possible mechanisms and consequences of this interaction. In the present report, it was demonstrated for the first time that DCs could be infected by P. brasiliensis and survive. Our results indicate that P. brasiliensis infection and purified gp43 lead to down-regulation of MHC-II and adhesion properties of immature DCs. The down-regulation was also observed in LPS-induced DCs maturation, where the expression of MHC-II, CD80, CD54 and CD40 were significantly inhibited in the presence of P. brasiliensis or gp43. These data show that the actions of P. brasiliensis on DCs could be mediated by gp43. In addition, an inhibition of IL-12 production by gp43 was observed in LPS-induced DC maturation. These results suggest that gp43 affects many functions of the host cells, indicating that this inhibition might be used by P. brasiliensis to reduce the effectiveness of the immune response, thus facilitating the establishment and fate of primary infection in susceptible host.
 
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Publishing Date
2009-05-21
 
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