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Master's Dissertation
DOI
https://doi.org/10.11606/D.99.2017.tde-29032017-091914
Document
Author
Full name
Alline Martins Rodrigues Santos
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2017
Supervisor
Committee
Goto, Hiro (President)
Alonso, Diego Peres
Starobinas, Nancy
Title in Portuguese
Efeito das lipoproteínas plasmáticas no parasitismo de células monocíticas humanas infectadas com Leishmania (Leishmania) infantum
Keywords in Portuguese
Arginina
Fator de crescimento Insulin-like I
Leishmania infantum
Lipoproteínas
Macrófagos
Abstract in Portuguese
Leishmaniose visceral (LV) é uma doença causada pelo protozoário Leishmania (Leishmania) infantum nas Américas que acomete células do sistema fagocítico mononuclear. Na doença ativa, ocorre redução nos níveis de lipoproteínas de alta densidade (HDL) e aumento nos níveis de colesterol total e triglicérides, sendo que a progressão da doença pode estar relacionada com essas alterações no nível de lipoproteínas. Desta forma, neste trabalho avaliamos: o efeito das lipoproteínas de muita baixa densidade (VLDL) e HDL no parasitismo de células de linhagem monocítica humana (THP-1) por L. (L.) infantum, a atividade da arginase e a expressão do mRNA do fator de crescimento insulina símile-I ("insulin-like growth factor-I" = IGF-I) e seu receptor ("insulin-like growth factor-I receptor" = IGF-IR). Células THP-1 foram infectadas por 6 h com promastigotas de L. (L.) infantum, na presença de 0,5% de soro com baixa concentração lipídica (infranadante) e na presença ou ausência das frações lipoprotéicas em diferentes concentrações. As células foram lavadas e mantidas depois em meio de cultura acrescido com infranadante por 24, 48 e 72 h. Quando as frações de VLDL e HDL foram adicionadas separadamente durante a incubação inicial o parasitismo aumentou em relação ao controle. Quando as frações de VLDL e HDL foram adicionadas concomitantemente houve diminuição do parasitismo em relação ao controle, mas aumento inesperado da atividade da arginase, nos períodos de 24 e 48 h. A expressão do mRNA de IGF-I e IGF-IR mostrou uma diminuição nas células infectadas na presença e ausência das frações em relação às células não infectadas. Os resultados obtidos sugerem um papel importante de VLDL e HDL na infecção de células THP-1 por L. (L.) infantum.
Title in English
Effect of plasma lipoproteins on the parasitism of human monocytic cells infected with Leishmania (Leishmania) infantum
Keywords in English
Arginine
Insulin-like growth factor-I
Leishmania infantum
Lipoproteins
Macrophages
Abstract in English
Visceral leishmaniasis (VL) is a disease caused by the protozoan Leishmania (Leishmania) infantum in Americas that affects cells of the mononuclear phagocytic system. During active disease reduction in high density lipoprotein (HDL) and increase in total cholesterol and triglyceride levels are observed. Thus in this study we evaluated the effect of very low density lipoprotein (VLDL) and HDL on the parasitism of cells of human monocytic line (THP-1) by L. (L.) infantum, the arginase activity and insulin-like growth factor-I (IGF-I) and insulin-like growth factor-I receptor (IGF-IR) mRNA expressions. THP-1 cells were infected for 6 h with L. (L.) infantum promastigotes in the presence of 0.5% low lipid concentration serum (infranatant) in the presence or absence of lipoprotein fractions at different concentrations. The cells were washed and then maintained in medium with infranatant for 24, 48 and 72 h. When VLDL and HDL were added separately the parasitism increased when compared with the control. When VLDL and HDL were added concomitantly the parasitism decreased in relation to the control but with unexpected increase in arginase activity. The evaluation of IGF-I and IGF-IR mRNA expression showed a decrease in the cells infected in the presence and absence of the fractions comparing with the uninfected cells. The results suggest an important effect of VLDL and HDL in the infection of THP-1 cells by L. (L.) infantum.
 
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AllineCorrigida.pdf (1.22 Mbytes)
Publishing Date
2017-03-30
 
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