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Ex Vivo Production (ex + vivo_production)
Selected AbstractsRelationship of in vivo and ex vivo levels of TH1 and TH2 cytokines with viremia in HAART patients with and without opportunistic infectionsJOURNAL OF MEDICAL VIROLOGY, Issue 4 2006Sardar Sindhu Abstract TH1/TH2 cytokines' imbalance is critical to HIV-1 progression and pathogenesis. Opportunistic infections-related cytokine perturbations in the setting of highly active antiretroviral therapy (HAART) are unclear. The objective of this cross-sectional study was to identify the relationship between TH1/TH2 cytokines and viremia in HAART patients with/without opportunistic infections. Sera from 17 HAART patients with and 43 without opportunistic infections, and 20 HIV-seronegative controls were used to measure the levels of IL-2, IFN-,, IL-4, and IL-10 proteins and mRNAs by ELISA and RNase protection assays, respectively. Ex vivo cytokine production by the CD4+/CD8+ T cells from four low and four high viremia patients randomly selected from non-opportunistic infection group was also evaluated. Serum IL-2 and IFN-, levels were lower (P,<,0.05) in patients than controls; this reduction was more pronounced for IFN-, in non-opportunistic infection patients. IL-4 and IL-10 were higher in patients than controls; this elevation was more remarkable in patients with opportunistic infections. Serum TH1/TH2 cytokine levels correlated with viremia. In vitro cytokine production assays showed that CD4+ T cells from low viremia patients mainly produced IL-2 and IFN-,, CD8+ T cells from high viremia patients produced IL-4, and both subsets comparably produced IL-10 in patients with similar viremia. Positive correlations between sera/supernatant proteins and cellular mRNAs were also found statistically significant (P,<,0.05). It was therefore concluded that in vivo TH1/TH2 cytokine levels in HAART patients and their ex vivo production by the CD4+/CD8+ T cells correlated with viremia and were also modulated by the presence of opportunistic infections in these patients. J. Med. Virol. 78:431,439, 2006. © 2006 Wiley-Liss, Inc. [source] Interleukin-1 gene cluster variants with innate cytokine production profiles and osteoarthritis in subjects from the Genetics, Osteoarthritis and Progression StudyARTHRITIS & RHEUMATISM, Issue 4 2010Ingrid Meulenbelt Objective To assess whether genetic variation in the interleukin-1 (IL-1) gene cluster contributes to familial osteoarthritis (OA) by influencing innate ex vivo production of IL-1, or IL-1 receptor antagonist (IL-1Ra). Methods Innate ex vivo IL-1, and IL-1Ra production upon lipopolysaccharide (LPS) stimulation of whole blood cells was measured in subjects from the Genetics, Osteoarthritis and Progression (GARP) Study, which includes sibling pairs in which at least one sibling has symptomatic OA at multiple sites. Radiographic OA (ROA) was assessed by Kellgren/Lawrence score. Subjects from the GARP Study and controls from the Rotterdam Study were genotyped for 7 single-nucleotide polymorphisms (SNPs) encompassing the IL-1 gene cluster on chromosome 2q13. Linkage disequilibrium analysis and genotype and haplotype association analysis were performed to assess the relationship between the IL-1 gene cluster SNPs, innate ex vivo cytokine production, and OA. Results Among subjects in the GARP Study, the haplotype variable-number tandem repeat in intron 2/T+8006C/T+11100C 2/2/1 of the IL1RN gene was significantly associated with reduced innate ex vivo bioavailability of IL-1, upon LPS stimulation (P = 0.026) and with ROA at the highest number of joint locations. Conclusion These results show that genetic variation at the IL-1 gene cluster is associated with lower IL-1, bioavailability and with OA at a large number of joint locations. The data further indicate that, among subjects with OA affecting the highest number of joints, the innate immune system may be activated, thereby obscuring possible underlying mechanisms. [source] Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokinesACTA NEUROLOGICA SCANDINAVICA, Issue 4 2010A. Vogelgesang Vogelgesang A, Rosenberg S, Skrzipek S, Bröker BM, Dressel A. Mitoxantrone treatment in multiple sclerosis induces TH2-type cytokines. Acta Neurol Scand: 2010: 122: 237,243. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objectives,,, Mitoxantrone is a cytotoxic drug with immune modulatory properties used in the treatment of progressive forms of multiple sclerosis (MS). We explored the effect of mitoxantrone treatment in MS patients on cytokine patterns induced in peripheral blood mononuclear cells (PBMC) and T-cell subsets ex vivo. Materials and methods,,, Blood was obtained before mitoxantrone infusion and 6, 12 and 18 days thereafter. Proliferation and prototypic TH1-, TH17- and TH2-type cytokines were determined following in vitro stimulation of PBMC, CD4+ and CD8+ T cells. In addition, a patient cohort receiving its first mitoxantrone treatment was cross-sectionally compared with a cohort of patients with more than 1 year of treatment. Results,,, Mitoxantrone treatment increased the ex vivo production of the TH2 cytokines interleukin-4 (IL-4; P < 0.05) and IL-5 (P < 0.001) in phytohemagglutinin-stimulated CD4+ T cells within 18 days of treatment. The cross-sectional study revealed that long-term treatment with mitoxantrone increased the inducibility of IL-4 and IL-5 secretion by PBMCs and CD4+ T cells even further. No significant changes were observed for interferon-,, tumour necrosis factor-,, IL-17 and IL-10. Mitoxantrone did not alter the proliferative capacity of ex vivo -stimulated T cells. Conclusion,,, Mitoxantrone treatment in MS enhances the inducibility of TH2-type cytokines, which may contribute to its beneficial effects in MS. [source] A mouse model of lupin allergyCLINICAL & EXPERIMENTAL ALLERGY, Issue 8 2009N. E. Vinje Summary Background Lupin has been introduced as a new food ingredient in an increasing number of European countries, resulting in reports of allergic reactions mostly due to cross-reactions in peanut-allergic individuals. Some cases of primary lupin allergy have also been reported. Objective The aim of our study was to develop a food allergy model of lupin in mice with anaphylaxis as the endpoint and further, to develop an approach to estimate the allergen dose inducing maximal sensitization using a statistical design requiring a limited number of animals. Methods Mice were immunized by intragastric gavage using cholera toxin as an adjuvant. A two-compartment response surface design with IgE as the main variable was used to estimate the maximal sensitizing dose of lupin in the model. This estimated dose was further used to evaluate the model. The mice were challenged with a high dose of lupin and signs of an anaphylactic reaction were observed. Antibody reactions (IgE and IgG2a), serum mast cell protease [mouse mast cell protease-1 (MMCP-1)] and ex vivo production of cytokines (IL-4, IL-5 and IFN-,) by spleen cells were measured. An immunoblot with regard to IgE binding was also performed. Results The dose that elicited the maximal sensitization measured as IgE was 5.7 mg lupin protein per immunization. Mice that received this dose developed anaphylactic reactions upon challenge, IgE against several proteins in the lupin extract, and high levels of MMCP-1, and showed a general shift towards a T-helper type 2 response. Post-challenge serum MMCP-1 levels corresponded to the seriousness of the anaphylactic reactions. Conclusion We have established a mouse model with clinical symptoms of lupin allergy, with an optimized dose of lupin protein. A statistical design that can be used to determine an optimal immunization dose with the use of a minimum of laboratory animals is described. [source] | ||||||||||