At first glance, the biological function of globoside (Gb) clusters appears to be that of glycosphingolipid (GSL) receptors for bacterial toxins that mediate host-pathogen interaction. Indeed, certain bacterial toxin families have been evolutionarily arranged so that they can enter eukaryotic cells through GSL receptors. A closer look reveals this molecular arrangement allocated on a variety of eukaryotic cell membranes, with its role revolving around physiological regulation and pathological processes. What makes Gb such a ubiquitous functional arrangement? Perhaps its peculiarity is underpinned by the molecular structure itself, the nature of Gb-bound ligands, or the intracellular trafficking unleashed by those ligands. Moreover, Gb biological conspicuousness may not lie on intrinsic properties or on its enzymatic synthesis/degradation pathways. The present review traverses these biological aspects, focusing mainly on globotriaosylceramide (Gb3), a GSL molecule present in cell membranes of distinct cell types, and proposes a wrap-up discussion with a phylogenetic view and the physiological and pathological functional alternatives.

Nutrition quality could be one of the reasons why, in the face of a Shiga toxin-producing enterohemorrhagic Escherichia coli outbreak, some patients experience more profound deleterious effects than others, including unfortunate deaths. Thus, the aim of this study was to determine whether high-fat and/or high-carbohydrate diets could negatively modulate the deleterious action of Shiga toxin 2 on ventral anterior and ventral lateral thalamic nuclei and the internal capsule, the neurological centers responsible for motor activity. Mice were fed a regular, high-fat, high-carbohydrate diet or a combination of both previous to the intravenous administration of Shiga toxin 2 or vehicle. Four days after intravenous administration, mice were subjected to behavioral tests and then sacrificed for histological and immunofluorescence assays to determine alterations in the neurovascular unit at the cellular and functional levels. Statistical analysis was performed using one-way analysis of variance followed by Bonferroni post hoc test. The criterion for significance was p = 0.0001 for all experiments. The high-fat and the high-carbohydrate diets significantly heightened the deleterious effect of Stx2, while the combination of both diets yielded the worst results, including endothelial glycocalyx and oligodendrocyte alterations, astrocyte and microglial reactivity, neurodegeneration, and motor and sensitivity impairment. In view of the results presented here, poor nutrition could negatively influence patients affected by Stx2 at a neurological level. Systemic effects, however, cannot be ruled out.

Background: Nutrition quality could be one of the reasons why, in the face of a Shiga toxin-producing enterohaemorrhagic Escherichia coli outbreak, some patients experience more profound deleterious effects than others, including unfortunate deaths. Thus, the aim of this study was to determine whether high-fat and/or high-carbohydrate diets could negatively modulate the deleterious action of Shiga toxin 2 on ventral anterior and ventral lateral thalamic nuclei and the internal capsule, the neurological centers responsible for motor activity. Methods: Mice were fed a regular, high-fat, high-carbohydrate diet or a combination of both previous to the intravenous administration of Shiga toxin 2 or vehicle. Four days after intravenous administration, mice were subjected to behavioral tests and then sacrificed for histological and immunofluorescence assays to determine alterations in the neurovascular unit at the cellular and functional levels. Statistical analysis was performed using one-way analysis of variance followed by Bonferroni post hoc test. The criterion for significance was p = 0.0001 for all experiments. Results: The high-fat and the high-carbohydrate diets significantly heightened the deleterious effect of Stx2, while the combination of both diets yielded the worst results, including endothelial glycocalyx and oligodendrocyte alterations, astrocyte and microglial reactivity, neurodegeneration, and motor and sensitivity impairment. Conclusions: In view of the results presented here, poor nutrition could negatively influence patients affected by Stx2 at a neurological level. Systemic effects, however, cannot be ruled out.