Effect of Magnesium Deficiency on Interleukin Production by Fisher Rats: Effect of Interleukins on Reduced in vitro Lymphocyte Responses to Concanavalin A and Lipopolysaccharide

Yiangou, Minas; Hadjipetrou-Kourounakis, L

doi:10.1159/000234949

Cited by 10 publications

(5 citation statements)

References 18 publications

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“…After counting splenocytes with a haemocytometer these were cultured (2 × 10 5 cells/well) in triplicates in 0.2 ml of RPMI-1640 complete medium [33] in the presence or absence of antigen (agPrP: 125 µg/ml; sPrP: 125 µg/ml; Ger: 125 µg/ml) or positive controls (concanavalin A, ConA, 0.5 µg/ml and lipopolysaccharide, LPS, 5 µg/ml) for 72 h at 37°C and 5% v/v CO 2 atmosphere. During the last 18 h, 0.04 µCi tritiated thymidine per well was added, and splenocyte proliferation was determined by tritiated thymidine incorporation using a β-counter.…”

Section: Methodsmentioning

confidence: 99%

Immunization with Recombinant Prion Protein Leads to Partial Protection in a Murine Model of TSEs through a Novel Mechanism

et al. 2013

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Transmissible spongiform encephalopathies are neurodegenerative diseases, which despite fervent research remain incurable. Immunization approaches have shown great potential at providing protection, however tolerance effects hamper active immunization protocols. In this study we evaluated the antigenic potential of various forms of recombinant murine prion protein and estimated their protective efficacy in a mouse model of prion diseases. One of the forms tested provided a significant elongation of survival interval. The elongation was mediated via an acute depletion of mature follicular dendritic cells, which are associated with propagation of the prion infectious agent in the periphery and in part to the development of humoral immunity against prion protein. This unprecedented result could offer new strategies for protection against transmissible encephalopathies as well as other diseases associated with follicular dendritic cells.

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Section: Methodsmentioning

confidence: 99%

Immunization with Recombinant Prion Protein Leads to Partial Protection in a Murine Model of TSEs through a Novel Mechanism

et al. 2013

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“…Splenocytes were cultured (2.5 Â 10 6 cells/well) in 1 ml of RPMI-1640 complete medium 19 in the presence or absence of 125 mg/ml of gliadin for 96 h at 371C and 5% CO2 atmosphere. During the last 18 h, 1 mCi tritiated thymidine per well was added, and splenocyte proliferation was determined by tritiated thymidine incorporation using a b-counter.…”

Section: Splenocyte Response To Gliadinmentioning

confidence: 99%

Gluten induces coeliac-like disease in sensitised mice involving IgA, CD71 and transglutaminase 2 interactions that are prevented by probiotics

Papista

Gerakopoulos

Kourelis

et al. 2012

Laboratory Investigation

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Coeliac disease (CD) is a malabsorptive enteropathy resulting from intolerance to gluten. Environmental factors and the microbiota are suggested to have critical roles in the onset of CD. The CD71 IgA receptor on epithelial cells is responsible for abnormal retrotranscytosis of IgA-gluten peptide complexes from the intestinal lumen into the lamina propria, inducing intestinal inflammation. However, understanding the role of gluten in the CD physiopathology has been hindered by the absence of relevant animal models. Here, we generated a mouse model for CD to study the factors controlling its pathogenesis as well as to investigate the influence of oral delivery of probiotics on disease development. Gluten sensitivity was established by feeding three generations of BALB/c mice a gluten-free diet (GÀ) followed by gluten challenge (G þ ) for 30 days. The G þ mice developed villous atrophy, crypt hyperplasia and infiltration of T cells and macrophages in the small intestine. Inflammation was associated with an overexpression of CD71 on the apical side of enterocytes and an increase of plasma cells producing IgA, which colocalised with the CD71. Moreover, IgA colocalised with the transglutaminase 2 (TG2), the production of which was increased in the lamina propria of G þ mice. These mice displayed increased production of cyclooxygenase-2 (COX-2), pro-inflammatory cytokines and IL-15, as well as anti-gliadin and anti-TG2 autoantibodies. The commensal flora-isolated presumptive probiotic Saccharomyces boulardii KK1 strain hydrolysed the 28-kDa a-gliadin fraction, and its oral delivery in G þ mice improved enteropathy development in association with decrease of epithelial cell CD71 expression and local cytokine production. In conclusion, the G þ BALB/c mouse represents a new mouse model for human CD based on histopathological features and expression of common biomarkers. The selected probiotic treatment reversing disease development will allow the study of the role of probiotics as a new therapeutic approach of CD.

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“…In each experiment, all mice were injected at the same time (9:00-10:00 a.m.) and tissues were removed at the indicated times following each treatment. Peritoneal macrophages were isolated as described previously (Rokita et al, 1987;Yiangou & Hadjipetrou-Kourounakis, 1989). After the final wash, the cells were pelleted and RNA was isolated immediately by use of the RNAzol B kit.…”

Section: Methodsmentioning

confidence: 99%

Induction of several acute-phase protein genes by heavy metals: a new class of metal-responsive genes

Yiangou

Carter

et al. 1991

Biochemistry

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Acute-phase reactants, metallothioneins, and heat-shock proteins are the products of three families of genes that respond to glucocorticoids and cytokines. Metallothioneins and heat-shock proteins, however, are also stimulated by heavy metals, whereas very little is known about the effect of heavy metals on acute-phase-reactant genes. We have studied the effect of heavy metals (Hg, Cd, Pb, Cu, Ni, and Zn) and Mg on the acute-phase reactants alpha 1-acid glycoprotein, C-reactive protein, alpha 1-antitrypsin and alpha 1-antichymotrypsin. alpha 1-Acid glycoprotein and C-reactive protein mRNA levels were increased severalfold in livers of heavy-metal-treated Balb/c mice. The strongest induction was mediated by Hg, followed in order of response by Cd greater than Pb greater than Cu greater than Ni greater than Zn greater than Mg. None of the metals affected the mRNA levels of albumin, alpha 1-antitrypsin, and alpha 1-antichymotrypsin. Furthermore, failure to repress albumin, a negative acute-phase reactant, indicated that the induction of these genes was not due to a metal-mediated inflammatory response. The metals also induced alpha 1-acid glycoprotein and C-reactive protein in adrenalectomized animals, indicating that induction by the heavy metals is not mediated by the glucocorticoid induction pathway. Sequence analysis has revealed a region of homology to metal-responsive elements in the alpha 1-acid glycoprotein and C-reactive protein promoters. Additionally, an alpha 1-acid glycoprotein expression vector, pAGP(-595)CAT, responded to Hg and Cd when transfected into human HepG2 cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of Magnesium Deficiency on Interleukin Production by Fisher Rats: Effect of Interleukins on Reduced in vitro Lymphocyte Responses to Concanavalin A and Lipopolysaccharide

Cited by 10 publications

References 18 publications

Immunization with Recombinant Prion Protein Leads to Partial Protection in a Murine Model of TSEs through a Novel Mechanism

Immunization with Recombinant Prion Protein Leads to Partial Protection in a Murine Model of TSEs through a Novel Mechanism

Gluten induces coeliac-like disease in sensitised mice involving IgA, CD71 and transglutaminase 2 interactions that are prevented by probiotics

Induction of several acute-phase protein genes by heavy metals: a new class of metal-responsive genes

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