Dados do Trabalho

Título

Evolution of lesions caused by Leishmania amazonensis in fatty acid binding protein 4- whole body depleted mice

Introdução

Leiahmania spp are protozoan parasites that cause leishmaniasis, a disease with two main clinical forms: cutaneous and visceral. Drugs available have several problems such as high toxicity and costs and the need for parenteral administration in most cases. Therefore, it is important to comprehend which mechanisms play a role in the establishment of the infection and the signaling proteins involved during this process. Based on this scenario, we investigated the role of fatty acid transporter protein type 4, FABP4, present in mammals and abundantly expressed in macrophages, the main host cell of Leishmania spp. Our previous in vitro studies showed that there is a reduction in the infection rate by L. amazonensis in the presence of a specific FABP4 inhibitor.

Objetivo (s)

Thus, the objective of this work was to analyze the progression of the in vivo infection of C57/BL6 mice deleted for fabp4 (KO) in comparison to wild-type (WT) mice.

Material e Métodos

Next, genotyping was performed to identify the knocked out animals and five animals were separated from each group for infection with 1x106 axenic amastigotes of L. amazonensis in the left hind footpad. The evolution of the infection was monitored for 10 weeks with measurement of the right and left hind footpads. After this period, the animals were euthanized and the footpads were weighed and used to extract amastigotes for limiting dilution. In addition, livers and spleens were weighed.

Resultados e Conclusão

Weekly measurements showed changes in the evolution of the infection, and up to the 8th week, KO animals had smaller lesions compared to WT. After this period, there was an inversion of the size of the lesions between the groups. Footpads images also revealed larger lesions with the presence of larger ulcers in the KO group. There was no significant difference in parasite load between groups. Our studies are being deepened to understand whether the absence of FABP4 protein alters the pattern of lesion evolution by L. amazonensis in C57/BL6 mice, revealing an essential macrophage’s signalling protein that may play a relevant role in controlling the infection.

Palavras-chave

in vivo, Leishmania, mice.

Agradecimentos

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