RESUMEN
BACKGROUND: Dengue virus causes dengue fever (DF)disease, transmitted by the mosquito Aedes aegypti. The symptoms could be severe and disable the affected individuals for weeks. The severe form, dengue hemorrhagic fever (DHF), can lead to death if not adequately attended to. Due to global warming, the vector mosquito will advance over new areas and expose more people to this disease over the next decades. Despite the severity, there are no treatments nor efficient vaccines available. Metabolomic studies have shown a new perspective to understand this disease better at a new molecular level. AIM OF REVIEW: Many published works rely on samples obtained from animal studies. This review will mainly focus on human samples and cell culture experiments to view how the dengue virus affects the metabolomic profile. KEY SCIENTIFIC CONCEPTS OF REVIEW: The review compiles the sample sources, metabolomic techniques used, the detected compounds, and how they behave in different DF stages. This disease causes a significant change in many metabolites, but some results are still conflicting between studies. The results gathered here show that metabolomic approaches prove to be an excellent and viable way to expand knowledge about DF.
Asunto(s)
Dengue/metabolismo , Metabolómica/métodos , Aedes , Aminoácidos/metabolismo , Animales , Metabolismo de los Hidratos de Carbono , Dengue/virología , Humanos , Metabolismo de los Lípidos , Mosquitos VectoresRESUMEN
Fungal recognition by Dectin-1 receptor triggers a series of cellular mechanisms involved in a protective activation of the immune system. In this study, we aimed to evaluate the participation of Dectin-1 receptor in the induction of IL-8, TNF-α, IL-12, IL-10 and IL-17A secretion by human monocytes activated with different cytokines, and challenged in vitro with Paracoccidioides brasiliensis (P. brasiliensis). Our results show that monocytes challenged with P. brasiliensis (Pb265) are able to produce IL-12, IL-8, IL-17, IL-10 and TNF-α. Dectin-1 receptor blockage decreased the IL-12, IL-17, IL-10 and TNF-α levels indicating the participation of such receptor in the induction of these cytokines. Only IL-8 production was not affected by the blockage. Cells activation with different cytokines showed that GM-CSF was able to induce secretion of all cytokines and the receptor blockage prior to the challenge also decreased the cytokine secretion, except IL-8. Monocytes activated with TNF-α promoted IL-8, IL-10 and TNF-α production, whereas stimulation with IFN-γ promoted mainly IL-12 and TNF-α. Thus, these findings bring new and important knowledge about Dectin-1 participation in cytokines production by monocytes challenged with Pb265.