Iron craftsmanship in Muweis, a town of the Meroe Empire: metal production and smithing

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Effects of Macronutrients on the In Vitro Production of ClpB, a Bacterial Mimetic Protein of α-MSH and Its Possible Role in Satiety Signaling

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Dietary salt exacerbates intestinal fibrosis in chronic TNBS colitis via fibroblasts activation

International audienceAbstract Intestinal fibrosis is a frequent complication in inflammatory bowel diseases (IBD). It is a challenge to identify environmental factors such as diet that may be driving this risk. Intestinal fibrosis result from accumulation of extracellular matrix (ECM) proteins secreted by myofibroblasts. Factors promoting intestinal fibrosis are unknown, but diet appears to be a critical component in its development. Consumption of salt above nutritional recommendations can exacerbate chronic inflammation. So far, high salt diet (HSD) have not been thoroughly investigated in the context of intestinal fibrosis associated to IBD. In the present study, we analyze the role of dietary salt in TNBS chronic colitis induced in rat, an intestinal fibrosis model, or in human colon fibroblast cells. Here, we have shown that high-salt diet exacerbates undernutrition and promoted ECM-associated proteins in fibroblasts. Taken together, our results suggested that dietary salt can activate intestinal fibroblasts, thereby contributing to exacerbation of intestinal fibrosis. Dietary salt may be considered as a putative environmental factor that drives intestinal fibrosis risk

Ghrelin inhibits autonomic response to gastric distension in rats by acting on vagal pathway

International audienceGhrelin is the only orexigenic peptide currently known and a potent prokinetic by promoting gastric motility but novel insights suggest that its role extends beyond satiety regulation. Whereas ghrelin was shown to provide somatic and colonic antinociception, its impact on gastric sensitivity is unknown even though stomach is a major ghrelin secreting tissue. Autonomic response to gastric mechanosensitivity was estimated by measuring blood pressure variation as a surrogate marker in response to gastric distension (GD) before and after ghrelin (or vehicle) administration. Involvement of spinal and vagal pathways in the ghrelin effect was studied by performing celiac ganglionectomy and subdiaphragmatic vagotomy respectively and by evaluating the expression of phosphorylated extracellular-regulated kinase 1/2 (p-ERK1/2) in dorsal root and nodose ganglia. Finally the phenotype of Ghrelin receptor expressing neurons within the nodose ganglia was determined by in situ hybridization and immunofluorescence. Ghrelin reduced blood pressure variation in response to GD except in vagotomized rats. Phosphorylated-ERK1/2 levels indicated that ghrelin reduced neuronal activation induced by GD in nodose ganglion. The effect of ghrelin on gastric mechanosensitivity was abolished by pre-treatment with antagonist [D-Lys3]-GHRP-6 (0.3 mg/kg i.v.). Immunofluorescence staining highlights the colocalization of Ghrelin receptor with ASIC3 and TRPV1 within gastric neurons of nodose ganglion. Ghrelin administration reduced autonomic response to gastric distension. This effect likely involved the Ghrelin receptor and vagal pathways

SPECT-computed tomography in rats with TNBS-induced colitis: A first step toward functional imaging

International audienceTo assess the feasibility of SPECT-computed tomography (CT) in rats with trinitrobenzene sulfonic acid (TNBS)-induced acute colitis and confront it with model inflammatory characteristics

PamR, a new MarR-like regulator affecting prophages and metabolic genes expression in <i>Bacillus subtilis</i>

<div><p><i>B</i>. <i>subtilis</i> adapts to changing environments by reprogramming its genetic expression through a variety of transcriptional regulators from the global transition state regulators that allow a complete resetting of the cell genetic expression, to stress specific regulators controlling only a limited number of key genes required for optimal adaptation. Among them, MarR-type transcriptional regulators are known to respond to a variety of stresses including antibiotics or oxidative stress, and to control catabolic or virulence gene expression. Here we report the characterization of the <i>ydcFGH</i> operon of <i>B</i>. <i>subtilis</i>, containing a putative MarR-type transcriptional regulator. Using a combination of molecular genetics and high-throughput approaches, we show that this regulator, renamed PamR, controls directly its own expression and influence the expression of large sets of prophage-related and metabolic genes. The extent of the regulon impacted by PamR suggests that this regulator reprograms the metabolic landscape of <i>B</i>. <i>subtilis</i> in response to a yet unknown signal.</p></div

Glutamine Restores Tight Junction Protein Claudin-1 Expression in Colonic Mucosa of Patients With Diarrhea-Predominant Irritable Bowel Syndrome

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The YdcH regulon.

<p>Pie charts summarizing genome-wide transcriptional profiling by RNAseq comparing gene expressions in a WT (ABS2005) and a Δ<i>ydcH</i> strain (ASEC56). The 363 genes retained (left chart) were reproducibly and statistically induced (182, right up) or repressed (181, right down) in the mutant compared to the wt by at least a two-fold factor. Genes were sorted by functional categories (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0189694#pone.0189694.s007" target="_blank">S5 Table</a> for complete results), then regrouped into families of functions: Metabolism (carbon sources, amino acids, lipids, nucleotides and other metabolic pathways; electron transport & ATP synthesis; transport of sugars and other metabolites), stress response, information processing (DNA replication, segmentation, modification, recombination and repair; RNA and protein synthesis, modification and degradation), cellular processes (cell division; cell envelope synthesis, modification and degradation; ion homeostasis), lifestyles (motility & chemotaxis; biofilms formation; competence; sporulation), prophages & mobile genetic elements, and unknown. Numbers indicate the number of gene for each category.</p

Dietary n-3 PUFA May Attenuate Experimental Colitis

International audienceBackground. Inflammatory bowel diseases (IBD) occurred in genetically predisposed people exposed to environmental triggers. Diet has long been suspected to contribute to the development of IBD. Supplementation with n-3 polyunsaturated fatty acids (PUFA) protects against intestinal inflammation in rodent models while clinical trials showed no benefits. We hypothesized that intervention timing is crucial and dietary fatty acid pattern may influence intestinal environment to modify inflammation genesis. The aim of this study was to evaluate the dietary effect of PUFA composition on intestinal inflammation. Methods. Animals received diet varying in their PUFA composition for four weeks before TNBS-induced colitis. Colon inflammatory markers and gut barrier function parameters were assessed. Inflammatory pathway PCR arrays were determined. Results. n-3 diet significantly decreased colon iNOS, COX-2 expression, IL-6 production, and LTB4 production but tended to decrease colon TNFα production () compared to control diet. Tight junction protein (claudin-1, occludin) expressions and MUC2 and TFF3 mRNA levels were not different among groups. n-9 diet also decreased colon IL-6 production (). Conclusions. Dietary n-3 PUFA influence colitis development by attenuating inflammatory markers. Further research is required to better define dietary advice with a scientific rationale

YdcH binds specifically to inverted repeats in the promoter region of <i>ydcFGH</i>.

<p>A. Sequence of the region upstream of the <i>ydcFGH</i> operon. The two identified IR are indicated as green arrows. The transcriptional upshift previously identified is indicated as “up”, putative -35, -10 and rbs sequences are underlined, and the <i>ydcF</i> orf is boxed. B. EMSAs (right panels) showing the specific binding of PamR to DNA fragments corresponding to the wild type (wt) and mutated (IR1*) <i>ydcF</i> promoter, and schematic representation of the corresponding area (left panel). IRs are drawn as facing triangles, plain for the wild types and hollowed for the mutated. The quantity of YdcH (in pmol) incubated with 0.1 pmol of labeled target DNA is indicated above each lane.</p