Intestinal and systemic illnesses have been linked to increased gut permeability. Bile acids, whose luminal profile can be altered in human disease, modulate intestinal paracellular We investigated the mechanism by which selected bile acids increase permeability using a validated vitro model. Human Caco-2 cells were grown monolayers challenged with panel of acids. Transepithelial electrical resistance luminal-to-basolateral fluxes 10-kDa Cascade blue-conjugated dextran used monitor...

Abstract Under conditions of short-term hormone deprivation, epidermal growth factor (EGF) induces DNA synthesis, cytoskeletal changes, and Src activation in MCF-7 LNCaP cells. These effects are drastically inhibited by pure estradiol or androgen antagonists, implicating a role the steroid receptors these findings. Interestingly, EGF triggers rapid association with receptor (AR) α (ERα) cells ERβ Here, we show that, through (EGFR) erb-B2, tyrosine phosphorylation ER preassociated AR, thereby...

<b>Background:</b> Gliadins, a family of wheat proteins, are central to the pathogenesis celiac disease (CD). In addition ‘immunogenic’ effects, gliadin directly affects cultured cells and intestine preparations, produces damage in vivo, via separate ‘toxic’ peptide, such as A-gliadin p31–43 (P31–43). <b>Aims:</b> Understanding molecular mechanisms underlying direct non T-cell mediated effects peptides, assessing their potential role promoting CD. <b>Method:</b> Gliadin were tested on number...

Abstract Treatment of metastatic renal cell carcinoma (mRCC) has improved significantly with the advent agents targeting mTOR pathway, such as temsirolimus and everolimus. However, their efficacy is thought to be limited by feedback loops crosstalk other pathways leading development drug resistance. As CXCR4–CXCL12–CXCR7 axis been described have a crucial role in cancer; between pathway chemokine receptor investigated human cancer cells. In SN12C A498, common CXCR4–CXCR7 ligand, CXCL12,...

Celiac disease (CD) is a chronic inflammatory caused by genetic predisposition to an abnormal T cell-mediated immune response the gluten in diet. Different environmental proinflammatory factors can influence and amplify gluten. The aim of this manuscript was study role enterocytes CD intestinal inflammation their different factors, such as gliadin viruses. Intestinal biopsies from patients on gluten-containing (GCD-CD) or gluten-free diet (GFD-CD) well potential (Pot-CD) before onset lesions...

Antibodies against gametes of the malarial parasite inhibit development in mosquito and curtail transmission malaria. We now report that a monoclonal antibody human malaria pathogen Plasmodium vivax antibodies induced during natural infections P. humans which suppress infectivity parasites to vector at high concentrations can, lower concentrations, have opposite effect enhance level infection mosquitoes. Infectivity enhancing effects up 12-fold were demonstrated when blocking immune sera...

Background and Objectives Damage to intestinal mucosa in celiac disease (CD) is mediated both by inflammation due adaptive innate immune responses, with IL-15 as a major mediator of the response, proliferation crypt enterocytes an early alteration CD causing crypts hyperplasia. We have previously shown that gliadin peptide P31-43 induces cell lines delaying degradation active epidermal growth factor receptor (EGFR) delayed maturation endocytic vesicles. increased intestine patients affected...

Background Celiac Disease (CD) is both a frequent disease (1∶100) and an interesting model of induced by food. It consists in immunogenic reaction to wheat gluten glutenins that has been found arise specific genetic background; however, this still only partially understood. Activation innate immunity gliadin peptides important component the early events disease. In particular so-called "toxic" A-gliadin peptide P31-43 induces several pleiotropic effects including Epidermal Growth Factor...

Abstract: Epidermal growth factor (EGF) stimulates DNA synthesis and cytoskeletal rearrangement in human breast cancer (MCF‐7) prostate (LNCaP) cells. Both effects are inhibited by estrogen (ICI 182,780) androgen (Casodex) antagonists. This supports the view that crosstalk exists between EGF estradiol (ER) (AR) receptors suggests these directly involved action. Our recent work shows ER phosphorylation on tyrosine promotes association of a complex EGFR, AR/ER, kinase Src. The assembly...

Several recent reports describe a role of probiotics as therapeutic approach for celiac disease (CD). Two undigested A-gliadin peptides, P31-43 and P57-68, are central to CD pathogenesis, inducing an innate adaptive immune response, respectively. They enter enterocytes localize vesicular compartment induce their toxic/immunogenics effects. In this article, we tested the effect probiotic Lactobacillus paracasei (LP) CBA L74 (International Depository Accession Number LMG P-24778), its...

Celiac disease (CD) is an autoimmune characterized by inflammation of the intestinal mucosa due to immune response wheat gliadins. Some gliadin peptides are resistant digestion (e.g., A-gliadin P31-43) and induce a stress/innate response, but reason why they dangerous in intestines patients with CD unknown. In present study, P31-43 activated IFN-α, mediator innate CD, intestine subjects enterocyte cell line, CaCo-2. cooperated viral ligand activate TLR7 pathway interfering endocytic...

Celiac disease (CD) is an autoimmune characterized by altered immune response stimulated gliadin peptides that are not digested and cause damage to the intestinal mucosa. The aim of this study was investigate whether postbiotic Lactobacillus paracasei (LP) could prevent action on mTOR, autophagy, inflammatory response. Most experiments performed were conducted epithelial cells Caco-2 treated with a peptic-tryptic digest (PTG) P31-43. Furthermore, we pretreated LP before treatment previously...

Inflammation of intestinal tissue in patients affected by celiac disease (CD) originates from the adaptive and innate immune responses elicited undigested gliadin fragments through molecular mechanisms not yet completely described. Undigested A-gliadin peptide P31-43 is central to CD pathogenesis, entering enterocytes vesicular compartments endocytosis inducing an response mucosa. This study focused on reasons why does behave as immunogenic agent. Once obtained NMR analysis,...

We previously identified a Neisseria flavescens strain in the duodenum of celiac disease (CD) patients that induced immune inflammation ex vivo duodenal mucosal explants and CaCo-2 cells. also found vesicular trafficking was delayed after CD-immunogenic P31-43 gliadin peptide-entered cells Lactobacillus paracasei CBA L74 (L. paracasei-CBA) supernatant reduced peptide entry. In this study, we evaluated if metabolism altered CD-N. flavescens-infected any alteration could be mitigated by...

Objective. Most of the recent studies suggest that oats are well tolerated by celiac disease (CD) patients. However, it is still possible different oat cultivars may display biological properties relevant for CD pathogenesis. We aimed to investigate and immunological two varieties, Avena genziana potenza, in relation their safety Material Methods. Phosphorylation extracellular signal-regulated kinase (ERK) trans-epithelial electrical resistance (TEER) were evaluated CaCo-2 cells treated with...

Celiac disease (CD) occurs frequently, and is caused by ingestion of prolamins from cereals in subjects with a genetic predisposition. The small intestinal damage depends on an stress/innate immune response to certain gliadin peptides (e.g., A-gliadin P31-43) association adaptive other P57-68). Gliadin peptide P31-43 affect epithelial growth factor receptor (EGFR) signaling CD enterocyte proliferation. reason why the proliferative responses are present not control intestine so far unknown....

Abstract Celiac Disease (CD) is an autoimmune disease characterized by inflammation of the intestinal mucosa due to immune response wheat gliadins. Some gliadin peptides (e.g., A-gliadin P57-68) induce adaptive Th1 pro-inflammatory response. Other P31-43) a stress/innate involving interleukin 15 (IL15) and interferon α (IFN-α). In present study, we describe stressed/inflamed celiac cellular phenotype in enterocytes fibroblasts probably alteration early-recycling endosomal system. cells are...

Celiac disease (CD) is a frequent inflammatory intestinal disease, with genetic background, caused by gliadin-containing food. Undigested gliadin peptides P31-43 and P57-68 induce innate adaptive T cell-mediated immune responses, respectively. Alterations in the cell shape actin cytoskeleton are present celiac enterocytes, rearrangements both CD mucosa lines. Cell maintained focal adhesions, sites of membrane attachment to extracellular matrix. The locus human Lipoma Preferred Partner (LPP)...

Abstract Alpha‐gliadin peptide 31–43 is considered to be the main responsible for innate immune response in celiac disease patients. Recent evidence indicates that rapidly enters cells and interacts with early endocytic vesicular compartment. However, mechanism of its uptake not completely understood. Our aim characterize, isolate identify possible cell surface proteins involved internalization by Caco‐2 cells. In this study, we used a chemical cross‐linker block on proteins, pulled‐down...

Coeliac disease is an increasingly recognised pathology, induced by the ingestion of gluten in genetically predisposed patients. Undigested gliadin peptide can induce adaptive and innate immune response that unleash typical intestinal mucosal alterations. A growing attention paid to alternative therapeutic approaches gluten-free diet: one these use probiotics and/or postbiotics. We performed lactic fermentation rice flour with without pH control, using Lactobacillus paracasei CBA L74 as...

Objectives: Potential celiac disease (CD) patients are at an increased risk to developing CD as indicated by positive CD-associated serology. We investigated in duodenal mucosa of such the presence both IL-21 and IL-17A role gliadin peptides IL-15 their expression. Methods: Duodenal biopsies from 76 active CD, 90 potential 58 control were analyzed for and/or production quantitative real-time PCR, immunohistochemistry, flow cytometry, ELISA. The receptor was western blot. fragments cultured...