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  • 1. Ghaderi, Mehran
    et al.
    Gambelunghe, Giovanni
    Tortoioli, Cristina
    Brozzetti, Annalisa
    Jatta, Ken
    Örebro University, School of Health and Medical Sciences.
    Gharizadeh, Baback
    De Bellis, Annamaria
    Pecori Giraldi, Francesca
    Terzolo, Massimo
    Betterle, Corrado
    Falorni, Alberto
    MHC2TA single nucleotide polymorphism and genetic risk for autoimmune adrenal insufficiency2006In: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 91, no 10, 4107-4111 p.Article in journal (Refereed)
    Abstract [en]

    CONTEXT: The polymorphism of class II HLA genes modulates the genetic risk for several endocrine autoimmune diseases. The constitutive class II expression on antigen-presenting cells is under the control of the MHC class II transactivator, encoded by the MHC2TA gene, which is mapped to chromosome 16p13. The MHC2TA -168 A-->G single nucleotide polymorphism (rs3087456) has been suggested to confer susceptibility to some autoimmune diseases. DESIGN: With the aim of testing whether this MHC2TA single nucleotide polymorphism is independently associated with autoimmune Addison's disease (AAD) and/or modulates the genetic risk conferred by DRB1-DQA1-DQB1 haplotypes, we analyzed DNA samples from 128 AAD patients and 406 healthy control subjects from continental Italy. RESULTS: Frequency of allele G of MHC2TA was significantly increased among AAD patients (39% alleles), compared with 29% in healthy controls (P = 0.003). Similarly, the frequency of AG+GG genotypes was significantly higher among AAD patients than among healthy control subjects, in both a codominant (P = 0.012) and a G-dominant model (P = 0.018). Multivariate logistic regression analysis showed that MHC2TA AG+GG continued to be positively associated with genetic risk for AAD (P = 0.028, odds ratio = 1.72, 95% confidence interval = 1.06-2.78), after correction for DRB1*03-DQA1*0501-DQB1*0201, DRB1*04 (not 0403)-DQA1*0301-DQB1*0302 and DRB1*0403. Similar results were obtained when the number of G alleles was included in the model (P = 0.004; odds ratio = 1.65, 95% confidence interval = 1.17-2.32). CONCLUSIONS: Our study provides the first demonstration of the association of the polymorphism of the MHC2TA gene with genetic risk for AAD that appears to be independent from the well-known association with the polymorphism of HLA class II genes.

  • 2.
    Jatta, Ken
    Örebro University, Department of Clinical Medicine.
    Inflammation in atherosclerosis2006Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Consequences of atherosclerosis may result in a number of diseases of the cardiovascular system that represent serious health problems and major causes of morbidity and mortality worldwide. Although it is initially considered as disease of fibro-lipid and thrombus deposition in the arterial wall, it also involves an ongoing inflammatory response.

    Normally, the inflammatory response is considered as a protective defence mechanism of the body. However, if the inflammation gets out of proportion to the threat it is dealing with, it may then result in a sustained chronic disorder and thus may underlie the initial stage of atherogenesis. The work of this thesis focuses on the expression of cytokines/chemokines and the vascular transcriptional response to inflammation, i.e. LPS in atherosclerosis. This has mainly been studied in animal models of atherosclerosis; consequently, we set out to investigate these events using human material in vitro (human carotid lesions).

    Employing quantitative analysis, we were able to detect a significant induction of protein and mRNA of the cytokines IL-1β, IL-6, IL-10 and TNF-α and the chemokines IL-8 and MCP-1 by LPS in both atherosclerotic and non-atherosclerotic vessels. In contrast, LPS induction of TNF-α, IL-1β and IL-10 was solely observed in the lesions, but not in normal arteries. In addition, the impact of IL-1 gene polymorphism on the risk of myocardial infarction (MI) was estimated by DNA genotyping of 387 survivors of a first MI and 387 sex and age-matched control subjects. We found no statistically significant differences in either genotypic distribution or allelic frequencies of IL-1β (-511) or IL-1Ra (VNTR) polymorphisms between first-time survivors of myocardial infarction and their age-matched healthy controls. Incontrast, our results demonstrated a strong association between the IL-1Ra genotype and severity of angiographically determined coronary artery disease in post-MI patients. To further investigate the vascular response to inflammation, we used gene array analysis to evaluate the human vascular transcriptional response to LPS of non-atherosclerotic human renal arteries compared to carotid lesions. In LPS treated renal arteries, 54% of the transcripts gave a detectable signal, where 4% were upregulated and 3.8% down-regulated. In the LPS stimulated carotid lesions, 44% of transcripts were detected. In this latter group, 5.1% of transcripts were increased and 3.3% decreased. Interestingly, a newly identified virus-inducible antiviral protein, CMV inducible gene 5/viperin (Cig5), was among the most strongly induced gene in both normal and atherosclerotic biopsies. Single gene analysis revealed viperin in the endothelium of human atherosclerotic lesions. Further, viperin was induced in vascular cells by inflammatory stimuli and CMV infection.

    In conclusion we show that atherosclerotic vessels produce more proinflammatory cytokines/chemokines than normal vessels. Interestingly, our results indicate that LPS enhances the expression of cytokines/chemokines in a similar pattern both in lesions and normal arteries. However, the response is stronger in atherosclerotic lesions. Furthermore, our results suggest that genetic polymorphisms within the IL-1Ra loci may influence the severity of CAD. Finally, the CMV inducible gene 5/viperin have been identified as a putative culprit molecule in vascular inflammation and atherosclerosis.

    List of papers
    1. Lipopolysaccharide-induced cytokine and chemokine expression in human carotid lesions
    Open this publication in new window or tab >>Lipopolysaccharide-induced cytokine and chemokine expression in human carotid lesions
    Show others...
    2005 (English)In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 42, no 3, 266-271 p.Article in journal (Refereed) Published
    Abstract [en]

    The release of cytokines and chemokines from activated immune-competent cells plays a crucial role in determining the pathology of the atherogenic progress. We investigated the effect of bacterial lipopolysaccharide (LPS) on cytokine/chemokine expression in carotid lesions and normal renal arteries. The lesions or renal arteries were incubated for 6 h at 37 degrees C in serum-free media treated with or without LPS. After LPS treatment, increased protein levels of IL-1beta, IL-6, IL-8, IL-10, TNF-alpha and MCP-1 were observed in the culture medium from the lesions measured with cytometric bead array. We were able to detect the induction of IL-1beta, IL-6, IL-8, IL-10, TNF-alpha and MCP-1 mRNA in the lesions after stimulation with LPS using real-time PCR. In renal arteries, LPS also induces mRNA expression of all chemokines and cytokines investigated with the exception of IL-6. However, LPS induces significantly higher levels of TNF-alpha, IL-1beta and IL-10 mRNA in lesions compared to renal arteries. The results suggest that infectious agents are capable of enhancing the production of cytokines/chemokines in an already ongoing inflammatory process such as in atherosclerosis, and that low levels of circulating LPS may affect the levels of pro-inflammatory cytokines much more in atherosclerotic vessels than in normal vessels and may contribute to the development of the atherosclerotic lesion.

    National Category
    Medical and Health Sciences
    Research subject
    Biomedicine
    Identifiers
    urn:nbn:se:oru:diva-3082 (URN)10.1159/000085721 (DOI)
    Available from: 2006-05-11 Created: 2006-05-11 Last updated: 2017-12-14Bibliographically approved
    2. The antiviral cytomegalovirus inducible gene 5/viperin is expressed in atherosclerosis and regulated by proinflammatory agents
    Open this publication in new window or tab >>The antiviral cytomegalovirus inducible gene 5/viperin is expressed in atherosclerosis and regulated by proinflammatory agents
    Show others...
    2005 (English)In: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 25, no 7, 113-116 p.Article in journal (Refereed) Published
    Abstract [en]

    OBJECTIVE:

    Inflammatory processes play an important role in atherosclerosis, and increasing evidence implies that microbial pathogens and proinflammatory cytokines are involved in the development and activation of atherosclerotic lesions. To find new inflammatory genes, we explored the vascular transcriptional response to an activator of innate immunity bacterial lipopolysaccharides (LPSs).

    METHODS AND RESULTS:

    Gene arrays identified the cytomegalovirus-inducible gene 5 (cig5)/viperin among the genes most potently induced by LPS in human vascular biopsies. Viperin was expressed by endothelial cells in atherosclerotic arteries and significantly elevated in atherosclerotic compared with normal arteries. In culture, cytomegalovirus infection, interferon-gamma, and LPS induced viperin expression.

    CONCLUSIONS:

    Viperin is expressed in atherosclerosis and induced in vascular cells by inflammatory stimuli and cytomegalovirus infection. The putative functions of viperin in atherosclerosis may relate to disease-associated microbes.

    National Category
    Medical and Health Sciences
    Research subject
    Biomedicine
    Identifiers
    urn:nbn:se:oru:diva-3083 (URN)10.1161/01.ATV.0000170130.85334.38 (DOI)15890971 (PubMedID)
    Available from: 2006-05-11 Created: 2006-05-11 Last updated: 2017-12-14Bibliographically approved
    3. Interleukin-1 receptor antagonist and the relation to cardiovascular disease
    Open this publication in new window or tab >>Interleukin-1 receptor antagonist and the relation to cardiovascular disease
    Show others...
    (English)Manuscript (Other academic)
    National Category
    Medical and Health Sciences
    Research subject
    Biomedicine
    Identifiers
    urn:nbn:se:oru:diva-3084 (URN)
    Available from: 2006-05-11 Created: 2006-05-11 Last updated: 2017-10-18Bibliographically approved
    4. Expression of IL-1b, IL-1R1 I and IL-1Ra in human aortic smooth muscle cells: effects of all-trans retinoic acid
    Open this publication in new window or tab >>Expression of IL-1b, IL-1R1 I and IL-1Ra in human aortic smooth muscle cells: effects of all-trans retinoic acid
    Show others...
    2006 (English)Manuscript (preprint) (Other academic)
    National Category
    Medical and Health Sciences
    Research subject
    Biomedicine
    Identifiers
    urn:nbn:se:oru:diva-3085 (URN)
    Available from: 2006-05-11 Created: 2006-05-11 Last updated: 2017-10-18Bibliographically approved
  • 3.
    Jatta, Ken
    et al.
    Örebro University, School of Health and Medical Sciences.
    Eliason, Gabriella
    Örebro University, School of Health and Medical Sciences.
    Portela-Gomes, Guida M.
    Grimelius, Lars
    Caro, Oscar
    Nilholm, Lennart
    Sirsjö, Allan
    Örebro University, School of Health and Medical Sciences.
    Piehl-Aulin, Karin
    Örebro University, School of Health and Medical Sciences.
    Abdel-Halim, Samy M.
    Örebro University, School of Health and Medical Sciences.
    Overexpression of von Hippel-Lindau protein in skeletal muscles of patients with chronic obstructive pulmonary disease2009In: Journal of Clinical Pathology, ISSN 0021-9746, E-ISSN 1472-4146, Vol. 62, no 1, 70-76 p.Article in journal (Refereed)
    Abstract [en]

    Background/aim: A Significant number of patients with chronic obstructive pulmonary disease (COPD) exhibit skeletal muscle wasting and decreased capillary area formation which have been correlated to increased mortality. The current study aimed to determine the molecular mechanisms mediating decreased capillary formation in COPD.

    Methods: Twenty-four COPD patients and twelve matching controls were recruited. COPD patients were divided into mild, moderate and severe groups according to GOLD (Global Initiative for Chronic Obstructive Lung Disease) criteria. Skeletal muscle biopsies were obtained from the tibialis anterior muscle. Fibre typing and capillary formation together with messenger RNA (mRNA) expression of hypoxia-inducible factors (HIF-1á and HIF-3á ), vascular endothelial growth factors (VEGF-A, -B and -C isoforms) and von Hippel Lindau (VHL) were determined. VHL expression and localization was further studied by immunohistochemistry.

    Results: Skeletal muscle capillary formation was significantly decreased with ascending disease severity. Compared to controls, a tendency to mRNA overexpression of HIF-1á, HIF-3á and VEGF isoforms was observed at mild and moderate COPD that decreased at the severe stage. By contrast, skeletal muscle biopsies from COPD patients exhibited significant overexpression of VHL both on the mRNA and protein levels by immunohistochemistry. VHL protein was further determined to be localized to satellite cells.

    Conclusions: Overexpression of VHL was identified in the skeletal muscle of patients with COPD. Increased VHL activity may exert a negative impact on transducing the hypoxic signal and may contribute to decreased capillarization in skeletal muscles of patients with COPD.

  • 4.
    Jatta, Ken
    et al.
    Örebro University, Department of Clinical Medicine.
    Olofsson, Peder
    Ghaderi, Mehran
    Samnegård, Ann
    Eriksson, Per
    Sirsjö, Allan
    Örebro University, Department of Clinical Medicine.
    Interleukin-1 receptor antagonist and the relation to cardiovascular diseaseManuscript (Other academic)
  • 5.
    Jatta, Ken
    et al.
    Örebro University, Department of Clinical Medicine.
    Wågsäter, Dick
    Örebro University, Department of Clinical Medicine.
    Norgren, Lars
    Stenberg, Björn
    Sirsjö, Allan
    Örebro University, Department of Clinical Medicine.
    Lipopolysaccharide-induced cytokine and chemokine expression in human carotid lesions2005In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 42, no 3, 266-271 p.Article in journal (Refereed)
    Abstract [en]

    The release of cytokines and chemokines from activated immune-competent cells plays a crucial role in determining the pathology of the atherogenic progress. We investigated the effect of bacterial lipopolysaccharide (LPS) on cytokine/chemokine expression in carotid lesions and normal renal arteries. The lesions or renal arteries were incubated for 6 h at 37 degrees C in serum-free media treated with or without LPS. After LPS treatment, increased protein levels of IL-1beta, IL-6, IL-8, IL-10, TNF-alpha and MCP-1 were observed in the culture medium from the lesions measured with cytometric bead array. We were able to detect the induction of IL-1beta, IL-6, IL-8, IL-10, TNF-alpha and MCP-1 mRNA in the lesions after stimulation with LPS using real-time PCR. In renal arteries, LPS also induces mRNA expression of all chemokines and cytokines investigated with the exception of IL-6. However, LPS induces significantly higher levels of TNF-alpha, IL-1beta and IL-10 mRNA in lesions compared to renal arteries. The results suggest that infectious agents are capable of enhancing the production of cytokines/chemokines in an already ongoing inflammatory process such as in atherosclerosis, and that low levels of circulating LPS may affect the levels of pro-inflammatory cytokines much more in atherosclerotic vessels than in normal vessels and may contribute to the development of the atherosclerotic lesion.

  • 6. Olofsson, P. S.
    et al.
    Sheikine, Y.
    Jatta, Ken
    Örebro University, School of Health and Medical Sciences.
    Ghaderi, M.
    Samnegård, A.
    Eriksson, P.
    Sirsjö, Allan
    Örebro University, School of Health and Medical Sciences.
    A functional interleukin-1 receptor antagonist polymorphism influences atherosclerosis development - The interleukin-1β: Interleukin-1 receptor antagonist balance in atherosclerosis2009In: Circulation Journal, ISSN 1346-9843, E-ISSN 1347-4820, Vol. 73, no 8, 1531-1536 p.Article in journal (Refereed)
    Abstract [en]

    Background: Interleukin (JL)-β plays a central role in inflammation and atherosclerosis, but levels of IL-1β, its natural antagonist, IL-1Ra, and their balance in human atherosclerotic lesions, are unknown. Knowledge of protein levels in atherosclerosis and the influence of a functional IL-1Rα polymorphism would increase the understanding of atherosclerosis pathogenesis.

    Methods and Results: Fresh and endotoxin-stimulated explanted human atherosclerotic and normal arteries were analyzed for IL-1β, IL-1Ra and IL-1 receptor 1 (IL-1R1) using TaqMan PCR and enzyme-linked immunosorbent assay. Two hundred forty-three survivors of a first myocardial infarction were genotyped for a polymorphism in IL-1Ra and their coronary atherosclerosis analyzed by using coronary angiography. Levels of IL-1β, IL-1Ra and IL-1R1 mRNA were significantly increased in atherosclerotic arteries compared with normal arteries. Endotoxin stimulation increased IL-1β levels more than IL-1Ra levels (ie, promoted a pro-inflammatory state). A polymorphism in IL-1Ra known to increase levels of IL-1Ra was associated with decreased mean coronary artery plaque area.

    Conclusions: Activation of innate immunity changed the balance between IL-1β and IL-1Ra in atherosclerotic arteries towards a more pro-inflammatory state. In line with this, the presence of an IL-1Ra intron 2 polymorphism known to increase IL-1Ra levels, and possibly the IL-1Ra:IL-1β ratio, was associated with reduced coronary atherosclerosis.

  • 7. Olofsson, Peder
    et al.
    Jatta, Ken
    Örebro University, Department of Clinical Medicine.
    Wågsäter, Dick
    Gredmark, Sara
    Hedin, Ulf
    Paulsson-Berne, Gabrielle
    Söderberg-Nauclér, Cecilia
    Hansson, Göran
    Sirsjö, Allan
    Örebro University, Department of Clinical Medicine.
    The antiviral cytomegalovirus inducible gene 5/viperin is expressed in atherosclerosis and regulated by proinflammatory agents2005In: Arteriosclerosis, Thrombosis and Vascular Biology, ISSN 1079-5642, E-ISSN 1524-4636, Vol. 25, no 7, 113-116 p.Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE:

    Inflammatory processes play an important role in atherosclerosis, and increasing evidence implies that microbial pathogens and proinflammatory cytokines are involved in the development and activation of atherosclerotic lesions. To find new inflammatory genes, we explored the vascular transcriptional response to an activator of innate immunity bacterial lipopolysaccharides (LPSs).

    METHODS AND RESULTS:

    Gene arrays identified the cytomegalovirus-inducible gene 5 (cig5)/viperin among the genes most potently induced by LPS in human vascular biopsies. Viperin was expressed by endothelial cells in atherosclerotic arteries and significantly elevated in atherosclerotic compared with normal arteries. In culture, cytomegalovirus infection, interferon-gamma, and LPS induced viperin expression.

    CONCLUSIONS:

    Viperin is expressed in atherosclerosis and induced in vascular cells by inflammatory stimuli and cytomegalovirus infection. The putative functions of viperin in atherosclerosis may relate to disease-associated microbes.

  • 8.
    Wågsäter, Dick
    et al.
    Örebro University, Department of Clinical Medicine.
    Jatta, Ken
    Örebro University, Department of Clinical Medicine.
    Ocaya, Pauline
    Örebro University, Department of Clinical Medicine.
    Dimberg, Jan
    Sirsjö, Allan
    Örebro University, Department of Clinical Medicine.
    Expression of IL-1b, IL-1R1 I and IL-1Ra in human aortic smooth muscle cells: effects of all-trans retinoic acid2006Manuscript (preprint) (Other academic)
  • 9.
    Wågsäter, Dick
    et al.
    Örebro University, Department of Clinical Medicine.
    Jatta, Ken
    Örebro University, Department of Clinical Medicine.
    Ocaya, Pauline
    Örebro University, Department of Clinical Medicine.
    Dimberg, Jan
    Sirsjö, Allan
    Örebro University, Department of Clinical Medicine.
    Expression of IL-1β, IL-1 receptor type I and IL-1 receptor antagonist in human aortic smooth muscle cells: effects of all-trans-retinoic acid2006In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 43, no 4, 377-382 p.Article in journal (Refereed)
    Abstract [en]

    The proinflammatory cytokine interleukin (IL)-1β and the IL-1 receptor antagonist are expressed by atherosclerotic plaques and may be linked to the development of atherosclerosis. Existing evidence shows that retinoids and their receptors are involved in inflammatory response and that they are found in atherosclerotic plaques. In all-trans-retinoic acid (atRA)-treated human aortic smooth muscle cells (AOSMC), significant increases in IL-1β levels were observed, compared with untreated cells. Examination of IL-1 receptor antagonist and IL-1 receptor type I levels did not show any difference between atRA-treated and -untreated AOSMC. The results show that atRA-treated AOSMC express both the precursor (33 kDa) and the active form (17 kDa) of the IL-1β protein. atRA-treated carotid lesions showed significantly elevated IL-1β mRNA levels (2.9 ± 2.33) compared with untreated lesions (2.0 ± 1.77; p < 0.05). These results support the role of atRA as a regulator of inflammation such as in atherosclerosis.

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