During its life cycle, Trypanosoma rangeli invades the hemolymph of its invertebrate host and colonizes hemocytes and salivary glands. The parasite cannot synthesize some lipid classes, and during its cycle, it depends on the uptake of these molecules from its vertebrate and invertebrate hosts to meet growth and differentiation requirements. However, until now, knowledge on how the parasite affects the lipid physiology of individual insect organs has been largely unknown. Herein, the biochemical and molecular dynamics of triatomine R. prolixus lipid metabolism in response to acute T. rangeli infection were investigated. Biochemical and microscopic assays revealed the lipid droplet profile and the levels of the different identified lipid classes. In addition, a qRT‒PCR approach was used to determine the expression profile of 6 protein-coding genes involved in the R. prolixus lipid physiology. We observed that triacylglycerol (TAG), monoacylglycerol (MAG), phosphatidylethanolamine (PE) and phosphatidylcholine (PC) levels in the fat body decreased in infected insects. On the other hand, high levels of free fatty acids were observed in the hemolymph during infection. Analysis by confocal microscopy revealed a decrease in lipid droplets size from infected fat bodies, and investigations by scanning electron microscopy revealed a significant number of parasites adhered to the surface of the organ. T. rangeli infection upregulated the transcript levels of the protein-coding gene for the acetyl-CoA carboxylase, the first enzyme in the de novo fatty acid synthesis pathway, responsible for the production of malonyl-CoA. On the other hand, downregulation of lipophorin receptor was observed. In conclusion, this study reveals a new set of molecular events that occur within the vector in response to the challenge imposed by the parasite.
Keywords: Fat body; Lipid metabolism; Lipophorin; Rhodnius prolixus; Trypanosoma rangeli.
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