Recovery of thalamic microstructural damage after Shiga toxin 2-associated hemolytic–uremic syndrome

Krämer, Julia; Deppe, Michael; Göbel, Kerstin; Tabelow, Karsten; Wiendl, Heinz; Meuth, Sven G.

doi:10.1016/j.jns.2015.06.045

Cited by 11 publications

(4 citation statements)

References 36 publications

(114 reference statements)

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“…VT2 is 60% identical but significantly less toxic than VT1 in cell culture (Fuller et al, 2011). VT2 binds Gb 3 with lower affinity (Nakajima et al, 2001) but VT2 causes increased toxicity in mice (Conrady et al, 2010;Fuller et al, 2011) and other animal models (Mizuguchi et al, 2001;Takahashi et al, 2008) with increased association with disease (Kawano et al, 2008), particularly neurological sequelae following EHEC infection (Trachtman et al, 2012;Kramer et al, 2015). The different toxicity potency is due to B subunit differences (Head et al, 1991).…”

Section: Ehec Toxinsmentioning

confidence: 99%

Verotoxin Receptor-Based Pathology and Therapies

Lingwood

2020

Front. Cell. Infect. Microbiol.

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Section: Ehec Toxinsmentioning

confidence: 99%

Verotoxin Receptor-Based Pathology and Therapies

Lingwood

2020

Front. Cell. Infect. Microbiol.

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Section: Introductionmentioning

confidence: 80%

“…The thalamus is among the brain areas most affected in patients with HUS encephalopathy (8,(14)(15)(16). Patients usually exhibit symmetrical hyperintensities of thalamic magnetic resonance imaging, which is consistent with thalamic damage (14)(15)(16). Neurological signs comprise alterations in consciousness, cognitive dysfunction attention, orientation, working or shortterm memory deficits , and apraxia.…”

Section: Introductionmentioning

confidence: 95%

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagicEscherichia coliShiga toxin 2

Arenas-Mosquera,

Cerny,

Cangelosi

et al. 2024

Preprint

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BackgroundNutrition quality could be one of the reasons why, in the face of a Shiga toxin-producing enterohaemorrhagicEscherichia colioutbreak, 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 Bonferronipost hoctest. 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.

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“…These genes encode not only transcription factors but also proteins involved in neuron differentiation, synaptic plasticity and intracellular signaling. Stx2 was reported to play a role in CNS damage [33][34][35]. Stx2 interacts with neurons and promotes structural changes in the cell membrane that may indicate the synaptic vesicle cycle [36].…”

Section: Discussionmentioning

confidence: 99%

Behavioral Sensitization Induced by Methamphetamine Causes Differential Alterations in Gene Expression and Histone Acetylation of the Prefrontal Cortex in Rats

Chen

Ding

et al. 2020

Preprint

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Background: Methamphetamine (METH) is one of the most widely abused illicit substances worldwide; unfortunately, its addiction mechanism remains unclear. Based on accumulating evidence, changes in gene expression and chromatin modifications might be related to the persistent effects of METH on the brain. In the present study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the changes in gene expression and histone acetylation in the prefrontal cortex (PFC) of adult rats.Methods: We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analyses to screen and identify changes in transcript levels and histone acetylation patterns. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) using qPCR and ChIP-PCR assays.Results: In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylated genes (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analyses, 24 genes may be involved in METH-induced behavioral sensitization, and 7 were confirmed using qPCR. We further examined the alterations in the levels of the ANP32A and POU3F2 transcripts and histone acetylation at different periods of METH-induced behavioral sensitization. H4 hyperacetylation contributed to the increased levels of ANP32A mRNA and H3/H4 hyperacetylation contributed to the increased levels of POU3F2 mRNA induced by METH challenge-induced behavioral sensitization, but not by acute METH exposure.Conclusions: The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alterations in gene expression caused by METH-induced behavioral sensitization.

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Recovery of thalamic microstructural damage after Shiga toxin 2-associated hemolytic–uremic syndrome

Cited by 11 publications

References 36 publications

Verotoxin Receptor-Based Pathology and Therapies

Verotoxin Receptor-Based Pathology and Therapies

High-fat and high-carbohydrate diets worsen the mouse brain susceptibility to damage produced by enterohemorrhagicEscherichia coliShiga toxin 2

Behavioral Sensitization Induced by Methamphetamine Causes Differential Alterations in Gene Expression and Histone Acetylation of the Prefrontal Cortex in Rats

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