Glucose metabolism sustains heme-induced Trypanosoma cruzi epimastigote growth in vitro.

Chagas disease is caused by the protozoan parasite, Trypanosoma cruzi. This parasite alternates between an insect vector and a mammalian host. T. cruzi epimastigotes reside in the insect vector and coexist with the blood components of the vertebrate host. The metabolic profile of T. cruzi has been extensively studied; however, changes in its metabolism in response to signaling molecules present in the vector are poorly understood. Heme acts as a physiological oxidant that triggers intense epimastigote proliferation and upregulates the expression of genes related to glycolysis and aerobic fermentation in vitro. Here, heme-cultured epimastigotes increased D-glucose consumption. In fact, heme-cultured parasites secreted more succinate (the end product of the so-called succinic fermentation) followed by glucose intake. Increased succinate levels reduced the extracellular pH, leading to acidification of the supernatant. However, the acidification and proliferation stimulated by heme was impaired when glycolysis was inhibited. Otherwise, when glucose amount is enhanced in supernatant, heme-cultured parasites increased its growth whereas the glucose depletion caused a delay in proliferation. Heme supplementation increased epimastigote electron transport system-related O2 consumption rates, while glucose addition reduced both the electron transport system-related O2 consumption rates and spare respiratory capacity, indicating a Crabtree-like effect. These results show that glycolysis predominated in heme-cultured epimastigotes over oxidative phosphorylation for energy supply when glucose is present to sustain its high proliferation in vitro. Furthermore, it provided an insight into the parasite biology in the vector environment that supply glucose and the digestion of blood generates free heme that can lead to the growth of T. cruzi epimastigotes.

Saliva NMR-Based Metabolomics in the War Against COVID-19.

COVID-19 is an emergent, worldwide public health concern. Joint efforts have been made by scientific communities of various fields to better understand the mechanisms of action of SARS-CoV-2. The need to understand the pathophysiological fingerprint and pathways of this disease make metabolomics-related approaches an indispensable tool for properly answering concerns relating to disease course. Determination of the metabolomic profile may help to explain the heterogeneous spectra of COVID-19 clinical phenotypes and be useful in monitoring disease progression as well as therapeutic treatments. In this sense, saliva has proven to be a strategic biofluid, owing not only to its appeal as a noninvasive sampling method but also due to the capacity of the virus to invade epithelial cells of the oral mucosa and salivary gland ducts via ACE2 receptors. Accordingly, important changes in metabolism have been described relating to COVID-19, indicating that metabolomics may open new avenues for understanding the pathophysiology of this disease, especially via longitudinal study designs. Thus, we discuss the importance of comprehending the SARS-CoV-2 salivary metabolomic fingerprint and also highlight the situation of Brazil on the frontlines of the war against COVID-19.