| 1. |
- Arakelyan, Arsen, et al.
(författare)
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Functional Genetic Polymorphisms of Monocyte Chemoattractant Protein 1 and C-C Chemokine Receptor Type 2 in Ischemic Stroke
- 2014
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Ingår i: Journal of Interferon and Cytokine Research. - New Rochelle, NY : Mary Ann Liebert. - 1079-9907 .- 1557-7465. ; 34:2, s. 100-105
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Tidskriftsartikel (refereegranskat)abstract
- Recent findings indicated that monocyte chemoattractant protein 1 (MCP1) and its C-C chemokine receptor type 2 (CCR2) play a key role in ischemic stroke (IS) progression. This study was aimed at evaluating the potential association of the MCP1 gene (MCP1) rs1024611 (-2518 A>G) and CCR2 gene (CCR2) rs1799864 (V64I; 190 G>A) functional single nucleotide polymorphisms (SNPs) with IS in the Armenian population. For the purpose of this study, genomic DNA samples of 100 patients with the first-episode IS and 115 healthy subjects (controls) were genotyped for the selected SNPs using a polymerase chain reaction with sequence-specific primers. The results obtained demonstrated that while the CCR2 rs1799864 SNP genotypes were equally distributed among patients and controls, the frequency and carriage rate of the of the MCP1 rs1024611*G minor allele were higher in patients. While a potential association between IS and CCR2 rs1799864 SNP was evaluated for the first time, the latest finding was in agreement with the earlier data reported for some other populations. In summary, this study revealed no association of CCR2 rs1799864 SNP with IS, and a positive association between G minor allele of MCP1 rs1024611 SNP and IS in the Armenian population. Based on the present and earlier reported data, we concluded that the minor G allele of the MCP1 rs1024611 SNP might be considered a risk factor for IS.
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| 2. |
- Bennermo, Marie, et al.
(författare)
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Genetic and environmental influences on the plasma interleukin-6 concentration in patients with a recent myocardial infarction : a case-control study
- 2011
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Ingår i: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 31:2, s. 259-264
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Tidskriftsartikel (refereegranskat)abstract
- The aim was to study the stimuli responsible for triggering and sustaining the plasma concentration of the inflammatory marker interleukin-6 (IL-6) in patients with a first myocardial infarction before the age of 60 and healthy control subjects matched for age and sex. The plasma IL-6 concentration, antibodies against Chlamydia pneumoniae, cytomegalovirus, Epstein-Barr virus, Helicobacter pylori, herpes simplex type 1 and 2, and genotype for the IL6-174 G>C single-nucleotide polymorphism were determined 3 months after the acute event. The results showed that patients had higher IL-6 levels than control subjects, whereas there were no differences regarding individual or total number (pathogen burden) of positive antibody tests against the different pathogens or IL6 genotype distribution. The plasma IL-6 concentration was associated with the number of positive antibody tests in patients and control subjects, whereas patients irrespective of IL6 genotype had increased IL-6. Multivariate analysis, including traditional coronary heart disease risk factors, antibodies against pathogens, and IL6 genotype, explained 17% of the variation of the plasma IL-6 concentration. Neither pathogen burden nor IL6 genotype did contribute to the variation of plasma IL-6 levels, whereas smoking, body-mass index, hypertension, case-control status, and age were determinants of the plasma IL-6 concentration.
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| 3. |
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| 4. |
- Eliasson, Mette, et al.
(författare)
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Characterization of Released Polypeptides During an Interferon-γ-Dependent Antibacterial Response in Airway Epithelial Cells.
- 2012
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Ingår i: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1557-7465 .- 1079-9907. ; 32:11, s. 524-533
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Tidskriftsartikel (refereegranskat)abstract
- When pathogenic bacteria breach the epithelial lining at mucosal surfaces, rapidly available innate immune mechanisms are critical to halt the infection. In the present study, we characterized the production of antibacterial polypeptides released by epithelial cells. IFN-γ, but neither TNF nor IL-1β alone, induced release of antibacterial activity to a cell culture medium, causing a lytic appearance of killed bacteria as revealed by electron microscopy. Addition of the protein streptococcal inhibitor of complement, derived from Streptococcus pyogenes, known for its ability to neutralize antimicrobial polypeptides (AMPs), reduced the antibacterial activity of the medium. Characterization of the antibacterial incubation medium using mass spectrometric approaches and ELISAs, displayed presence of several classical AMPs, antibacterial chemokines, as well as complement factors and proteases that may interfere with bacterial killing. Many were constitutively produced, that is, being released by cells incubated in a medium alone. While a combination of IFN-γ and TNF did not increase bacterial killing, the presence of TNF boosted the amounts and detectable number of AMPs, including antibacterial chemokines. However, the methods applied in the study failed to single out certain AMPs as critical mediators, but rather demonstrate the broad range of molecules involved. Since many AMPs are higly amphiphatic in nature (i.e., cationic and hydrophobic), it is possible that difficulties in optimizing recovery present limitations in the context investigated. The findings demonstrate that epithelial cells have a constitutive production of AMPs and that IFN-γ is an important inducer of an antibacterial response in which is likely to be a critical part of the innate host defense against pathogenic bacteria at mucosal surfaces.
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| 5. |
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| 6. |
- Morrison, David
(författare)
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Genomic Analysis and mRNA Expression of Equine Type I Interferon Genes
- 2013
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Ingår i: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 33, s. 746-759
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Tidskriftsartikel (refereegranskat)abstract
- This study aimed at identifying all of the type I interferon (IFN) genes of the horse and at monitoring their expression in equine cells on in vitro induction. We identified 32 putative type I IFN loci on horse chromosome 23 and an unplaced genomic scaffold. A phylogentic analysis characterized these into 8 different type I IFN classes, that is, putative functional genes for 6 IFN-, 4 IFN-, 8 IFN- (plus 4 pseudogenes), 3 IFN- (plus 1 pseudogene), 1 IFN- and 1 IFN-, plus 1 IFN- pseudogene, and 3 loci belonging to what has previously been called IFN-. Our analyses indicate that the IFN- genes are quite distinct from both IFN- and IFN-, and we refer to this type I IFN as IFN-. Results from cell cultures showed that leukocytes readily expressed IFN-, IFN-, IFN-, IFN-, and IFN- mRNA on induction with, for example, live virus; while fibroblasts only expressed IFN- mRNA on stimulation. IFN- or IFN- expression was not consistently induced in these cell cultures. Thus, the equine type I IFN family comprised 8 classes, 7 of which had putative functional genes, and mRNA expression of 5 was induced in vitro. Moreover, a relatively low number of IFN- subtypes was found in the horse compared with other eutherian mammals.
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| 7. |
- Skovbjerg, Susann, 1973, et al.
(författare)
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Gram-positive and gram-negative bacteria induce different patterns of cytokine production in human mononuclear cells irrespective of taxonomic relatedness.
- 2010
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Ingår i: Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research. - New York, USA : Mary Ann Liebert Inc. - 1557-7465 .- 1079-9907. ; 30:1, s. 23-32
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Tidskriftsartikel (refereegranskat)abstract
- Upon bacterial stimulation, tissue macrophages produce a variety of cytokines that orchestrate the immune response that clears the infection. We have shown that Gram-positives induce higher levels of interleukin-12 (IL-12), interferon-gamma (IFN-gamma), and tumor necrosis factor (TNF) from human peripheral blood mononuclear cells (PBMCs) than do Gram-negatives, which instead induce more of IL-6, IL-8, and IL-10. Here, we study whether these patterns follows or crosses taxonomic borders. PBMCs from blood donors were incubated with UV-inactivated bacteria representing 37 species from five phyla. IL-12, TNF, IL-1beta, IL-6, IL-8, and IL-10 were measured in the supernatants after 24 h and IFN-gamma after 5 days. Irrespective of phylogenetic position, Gram-positive bacteria induced much more IL-12 (nine times more on average) and IFN-gamma (seven times), more TNF (three times), and slightly more IL-1beta (1.5 times) than did Gram-negatives, which instead induced more IL-6 (1.5 times), IL-8 (1.9 times), and IL-10 (3.3 times) than did Gram-positives. A notable exception was the Gram-positive Listeria monocytogenes, which induced very little IL-12, IFN-gamma, and TNF. The results confirm the fundamental difference in innate immune responses to Gram-positive and Gram-negative bacteria, which crosses taxonomic borders and probably reflects differences in cell wall structure.
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| 8. |
- Sylvan, Staffan P. E., et al.
(författare)
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Modulation of Serum Interleukin-18 Concentrations and Hepatitis B Virus DNA Levels During Interferon Therapy in Patients with Hepatitis B e-Antigen-Positive Chronic Hepatitis B
- 2010
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Ingår i: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 30:12, s. 901-908
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Tidskriftsartikel (refereegranskat)abstract
- The aim of this study was (1) to determine plasma values of interleukin-18 (IL-18) in patients with different clinical manifestations of hepatitis B (HB) and (2) to analyze the correlation between presence of circulatory levels of IL-18 and levels of HB virus (HBV) DNA during interferon-alpha (IFN-alpha)-induced HBe seroconversion in patients with chronic HB (CHB). The IL-18 levels in serum did not significantly differ between healthy control subjects (99+/-25 pg/mL), HB-immune patients (85+/-33), and asymptomatic carriers of HB surface antigen (144+/-44 pg/mL). In contrast, anti-HBe (HBV DNA <10(4) copies/mL, 555+/-248, P<0.05), anti-HBe (HBV DNA >10(4) copies/mL, 280+/-85, P<0.05), and HBe-antigen-reactive (373+/-108, P<0.0001) patients with symptomatic CHB had significantly elevated levels in circulation compared with healthy control subjects (99+/-25 pg/mL). An inverse correlation was found between serum HBV DNA copies and IL-18 levels during therapy (r--0.54, P<0.001). We consistently observed an IFN-alpha-induced suppression of viral replication, which was followed by the alanine aminotransferase (ALT) flare. There was a significant increase in IL-18 production after the ALT flare, where the peak of IL-18 preceded or coincided with the time of HBe seroconversion in patients who cleared the virus. These results suggest that IL-18 is involved in the pathogenesis of CHB and that IFN-alpha therapy can augment the production of IL-18 in patients with CHB.
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