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Master's Dissertation
DOI
Document
Author
Full name
Anderson Guilherme dos Santos Barssotti
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2017
Supervisor
Committee
Goto, Hiro (President)
Galisteo Junior, Andrés Jimenez
Hiramoto, Roberto Mitsuyoshi
Title in Portuguese
Efeito do fator de crescimento insulina símile I na infecção in vitro de macrófagos peritoneais de camundongos por Leishmania (L.) amazonensis
Keywords in Portuguese
Expressão gênica
Fator de crescimento Insulin-Like I
Leishmania
Macrófagos
Óxido nítrico
Parasitismo
Abstract in Portuguese
Na infecção por Leishmania a resposta imune se inicia logo após a inoculação de promastigotas no indivíduo. Nesse contexto vai haver a participação de diversos fatores da resposta imune inata que vai direcionar para uma resposta imune adaptativa responsável pela evolução da doença. Um desses fatores que participa dessa interação parasito-hospedeiro é o fator de crescimento insulina-símile I (IGF-I). Foi demonstrado que o IGF-I extrínseco favorece a proliferação do parasito e progressão da infecção. No entanto, IGF-I está presente constitutivamente em macrófagos. Neste trabalho avaliamos a expressão do IGF-I, o parasitismo e a produção de óxido nítrico em macrófagos murinos infectado por Leishmania (L.) amazonensis e o efeito da inibição de IGF-I no parasitismo após o silenciamento do IGF-I por RNA de interferência. Macrófagos peritoneiais foram infectados por 2 e 4 horas com promastigotas de L. (L.) amazonensis na presença de soro fetal bovino (SFB) 5% e Albumina de Soro Bovino 0,5% (BSA) na presença ou ausência de small-interfering RNA (siRNA) de IGF-I e lipossoma (Lipo). As células foram lavadas e mantidas depois em meio de cultura por 24, 48 e 72 h. Quando o recombinante para IGF-I foi adicionado separadamente durante a incubação inicial o parasitismo aumentou em relação ao controle. Quando o siRNA foi adicionado houve diminuição na expressão de IGF-I e consequentemente diminuição no parasitismo em relação ao controle. Os resultados obtidos sugerem um papel importante de IGF-I na infecção de macrófagos peritoneais de camundongos murinos por Leishmania (l.) amazonensis.
Title in English
Effect of insulin-like growth factor I on the in vitro infection of mouse peritoneal macrophages by Leishmania L. amazonensis
Keywords in English
Gene expression
Insulin-like growth factor-I
Leishmania
Macrophages
Nitric oxide
Parasitism
Abstract in English
In Leishmania infection the immune response begins soon after the inoculation of promastigotes in the individual. In this context will be the participation of several factors of the innate immune response that will direct to an adaptive immune response responsible for the evolution of the disease. One of these factors that participates in this parasite-host interaction is the insulin-like growth factor I (IGF-I). It has been shown that extrinsic IGF-I favors parasite proliferation and infection progression. However, IGF-I is constitutively present in macrophages. In this work we evaluated the expression of IGF-I, parasitism and nitric oxide production in murine macrophages infected with Leishmania (L.) amazonensis and the effect of IGF-I inhibition on parasitism after IGF-I silencing by RNA from interference. Peritoneal macrophages were infected for 2 and 4 hours with L. (L.) amazonensis promastigotes in the presence of 5% fetal bovine serum (FBS) and 0.5% Bovine Serum Albumin (BSA) in the presence or absence of IGF-I small-interfering RNA (siRNA) and liposome (Lipo). Cells were washed and then maintained in culture medium for 24, 48 and 72 h. When the recombinant IGF-I was added separately during the initial incubation the parasitism increased relative to the control. When the siRNA was added there was a decrease in IGF-I expression and consequently a decrease in parasitism in relation to the control. The results obtained suggest an important role of IGF-I in the infection of murine mouse peritoneal macrophages by Leishmania (L.) amazonensis.
 
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BarssottiAGSparcial.pdf (597.75 Kbytes)
Release Date
2019-08-22
Publishing Date
2017-08-22
 
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