Search bioRxiv⌕ Search

Biology subjects

Cangelosi, A.

Publications and source records attributed to Cangelosi, A..

3 recordsLinked to original sources

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagic Escherichia coli Shiga toxin 2

BackgroundNutrition 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. MethodsMice 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. ResultsThe 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. ConclusionsIn 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.

microbiology↗

Paradoxical decrease of imitation performance with age in children

AbstractWe studied the development of imitation ability in a cohort of 6-11-year-old children (N=174) with specific attention to error types and their cognitive interpretation. Participants imitated meaningless actions as if they were in front of a mirror (specularly). Actions varied across three levels of complexity (movements of a single limb, arm and leg of the same body side, or arm and leg of opposite sides). Overall performance improved with age. Among the most frequent error categories, side errors (movement imitated with the left instead of the right limb or vice-versa) paradoxically increased with age (from 9 years). Still, their sensitivity to complexity decreased with age. Thus, encoding two opposite body sides has high cognitive costs in younger children and smaller or null costs in older children. We interpreted these results in terms of the enhancement of Working Memory (WM) and body knowledge with age. When WM increases, it paradoxically drives older children to apply their superior body knowledge and imitate anatomically, producing side errors. Younger children are free from such interference because they still lack the necessary body knowledge and WM capacity. In conclusion, this study suggests that anatomical imitation becomes available in childrens cognitive repertoire from age nine due to increased body knowledge and WM capacity. Research HighlightsO_LIThe analysis of error types uncovers/illustrates the role of working memory and body knowledge in imitation. C_LIO_LIAs an effect of little working memory capacity, younger children pay a cognitive cost to encode opposite body sides and make "side errors". C_LIO_LIImitation performance improves with age, but side errors paradoxically increase in frequency due to greater ability to master body knowledge bringing to anatomical imitation. C_LIO_LIAnatomical imitation is available in childrens cognitive repertoire from age 9, as an effect of the development of body knowledge and working memory capacity. C_LI

animal behavior and cognition↗

Cognitive deficits found in a pro-inflammatory state are independent of ERK 1/2 signaling in the murine brain hippocampus treated with Shiga toxin 2 from enterohemorrhagic Escherichia Coli

Shiga toxin 2 (Stx2) from enterohemorrhagic Escherichia coli (EHEC) produces hemorrhagic colitis, hemolytic uremic syndrome (HUS) and acute encephalopathy. The mortality rate in HUS increases significantly when the central nervous system (CNS) is involved. Besides, EHEC also releases lipopolysaccharide (LPS). Many reports have described cognitive dysfunctions in HUS patients, the hippocampus being one of the brain areas targeted by EHEC infection. In this context, a translational murine model of encephalopathy was employed to establish the deleterious effects of Stx2 and the contribution of LPS in the hippocampus. Results demonstrate that systemic administration of a sublethal dose of Stx2 reduced memory index and produced depression like behavior, pro-inflammatory cytokine release and NF-kB activation independent of the ERK 1/2 signaling pathway. On the other hand, LPS activated NF-kB dependent on ERK 1/2 signaling pathway. Cotreatment of Stx2 with LPS aggravated the pathologic state, while dexamethasone treatment succeeded in preventing behavioral alterations. Our present work suggests that the use of drugs such as corticosteroids or NF-kB signaling inhibitors may serve as neuroprotectors from EHEC infection.

pathology↗