Avaliação do efeito da expressão do gene da interleucina 32 (IL-32) humana em modelo murino de infecção por Leishmania (Leishmania) amazonensis
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2016-08-24
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Universidade Federal de Goiás
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IL-32 is a proinflammatory cytokine which has different isoforms. IL-32γ isoform is the most
powerful and was detected in lesions of patients with cutaneous leishmaniasis. Murine cells
respond to IL-32, however mice lack the gene for this cytokine. To understand the role of IL-
32 in Leishmania (L.) amazonensis, we used transgenic mice for human IL-32γ (IL-32γTg).
C57BL/6 mice (WT) and C57BL/6 IL-32γTg were infected with L. amazonensis promastigotes
in the ear. The lesion development was followed weekly with a digital caliper (measured in
mm of injury). After 3, 6 and 9 weeks, the animals were euthanized for tissue parasitism
analysis by the limiting dilution technique, in infected ears, draining lymph node and spleen of
mice. The draining lymph node cells were incubated (48 h) in the presence or absence of L.
amazonensis antigen (Ag) for analysis of cytokines by ELISA. IL-32γTg mice present IL-32
production in spleen, liver, lymph node and ear. IL-32γTg mice have a lower injury than the
WT mice during the third week of infection. From the 5th to the 9th week of infection, the two
groups had similar lesion development profiles. Interestingly, in the 3rd week of infection, the
parasitic load in the lesion of IL-32γTg mice was 100 times greater than that of WT mice.
After three weeks, IL-32γTg mice maintained the same parasitic load up to nine weeks. In WT
mice, however, the number of parasites increased exponentially during weeks evaluated. The
parasite load in the spleen and lymph node was lower in IL-32γTg mice when compared with
WT mice. There was no difference in histological sections of the lesions in WT and IL-32γTg
mice infected with L. amazonensis. We did not observe differences between WT and IL-32γTg
groups on the product -10) by lymph node cells stimulated
with Ag, in the 3rd, 6th and 9th week of infection. Our data suggest that IL-32γ favors
infection by L. amazonensis in the early stages, allowing the growth of the parasites.
However, this cytokine seems to limit the growth and spread of parasites in the later stages
of infection. In vitro analyzes show the similar percentage of infected cells and the number of
parasites per infected cell in WT macrophages and IL-32γTg after 3 and 48h of infection with
L. amazonensis. However, the production of NO by macrophages seems to be lower in IL-
32γTg mouse cells during infection with L. amazonensis. Understanding the mechanisms by
which IL-32γ modulates Leishmania amazonensis infection in mice is essential to define the
components that control cutaneous leishmaniasis caused by this specie in humans.
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SILVA, M. V. T. Avaliação do efeito da expressão do gene da interleucina 32 (IL-32) humana em modelo murino de infecção por Leishmania (Leishmania) amazonensis. 2016. 81 f. Dissertação (Mestrado em Biologia da Relção Parasito-Hospedeiro) - Universidade Federal de Goiás, Goiânia, 2016.