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  • 1.
    El Marghani, Ahmed
    et al.
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Abuabaid, Hanan
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Kjellén, Peter
    Örebro universitet, Akademin för naturvetenskap och teknik.
    TOM1L is involved in a novel signaling pathway important for the IL-2 production in Jurkat T cells stimulated by CD3/CD28 CoLigation2009Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, s. 416298-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    TOM1L (target of Myb-1 Like) was identified as a binding partner for the full length and catalytically-active Lck in a yeast 2-hybrid screening assay. Here we show that in Jurkat T cells stimulated by CD3/CD28 coligation where the expression of TOM1L is reduced by lenti virus mediated-siRNA results in a dramatically lower IL-2 production. The production of IL-2 in siRNA treated cells stimulated with PMA/ionomycin was not affected indicating an involvement of TOM1L in a pathway proximal of TCR and CD28. The coexpression of Fyn with TOM1L increased the level of the phosphorylated form of Fyn indicating that TOM1L has the ability to activate Fyn. The ability of TOM1L to activate Fyn was further shown in a kinase assay using angiotensin II as a substrate. By confocal microscopy, we show that the expression of TOM1L in non-treated HeLa and SK-N-SH cells colocalizes with the mitochondrial membrane but not with lysosomal compartments or the trans-Golgi network. Furthermore, we show that the over-expression of TOM1L in Jurkat cells causes an increase of the STAT3 expression. Based on our results, we here propose that TOM1L is involved in a novel signaling pathway that is important for the IL-2 production in T cells. Copyright (C) 2009 Ahmed Elmarghani et al.

  • 2.
    Gunaltay, Sezin
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Kumawat, Ashok Kumar
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Institute of Infection, College of Medical, Veterinary & Life Sciences, University of Glasgow, Glasgow, United Kingdom.
    Nyhlin, Nils
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län.
    Bohr, Johan
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län.
    Tysk, Curt
    Region Örebro län. Division of Gastroenterology, Department of Medicine, Örebro University, Örebro, Sweden.
    Hultgren, Olof
    Region Örebro län.
    Hultgren-Hörnquist, Elisabeth
    Örebro universitet, Institutionen för läkarutbildning.
    Enhanced levels of chemokines and their receptors in the colon of microscopic colitis patients indicate mixed immune cell recruitment2015Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikkel-id 132458Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Microscopic colitis (MC), comprising collagenous colitis (CC) and lymphocytic colitis (LC), is a common cause of chronic diarrhea. Various immune cell infiltrations in the epithelium and lamina propria are seen in MC immunopathology. We compared gene and protein expressions of different immune cell attracting chemokines and their receptors in colon biopsies from MC patients in active disease or histopathological remission (CC/LC-HR) with controls, using qRT-PCR and Luminex, respectively. CC and LC patients with active disease demonstrated a mixed chemokine profile with significantly enhanced gene and/or protein expressions of the chemokines CCL2, CCL3, CCL4, CCL5, CCL7, CCL22, CXCL8, CXCL9, CXCL10, CXCL11, and CX(3)CL1 and the receptors CCR2, CCR3, CCR4, CXCR1, CXCR2, and CX(3)CR1. Enhanced chemokine/chemokine receptor gene and protein levels in LC-HR patients were similar to LC patients, whereas CC-HR patients demonstrated almost normalized levels. These findings expand the current understanding of the involvement of various immune cells in MC immunopathology and endorse chemokines as potential diagnostic markers as well as therapeutic candidates. Moreover, this study further supports the hypothesis that CC and LC are two different entities due to differences in their immunoregulatory responses.

  • 3.
    Hedbrant, Alexander
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Andersson, Lena
    Region Örebro län. Örebro universitet, Institutionen för medicinska vetenskaper. Department of Occupational and Environmental Medicine.
    Bryngelsson, Ing-Liss
    Department of Occupational and Environmental Medicine, Örebro University Hospital, Örebro, Sweden.
    Eklund, Daniel
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Westberg, Håkan
    Department of Medical Sciences, School of Medicine and Health, Örebro University, Örebro, Sweden; Inflammatory Response and Infection Susceptibility Centre (iRiSC), Örebro University, Örebro, Sweden; Department of Occupational and Environmental Medicine, Örebro University Hospital, Örebro, Sweden.
    Särndahl, Eva
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Persson, Alexander
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers2020Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikkel-id 8490908Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Purpose: To study the association between inhalation of particulate matter or quartz in Swedish iron foundries and the effects on NLRP3 inflammasome activation. 

    Methods: Particle exposure measurements were performed during an eight-hour work day for 85 foundry workers at three Swedish iron foundries. Personal sampling was used for measurement of respirable quartz and dust and stationary measurements to obtain exposure measurements for inhalable dust and PM10. The NLRP3 inflammasome markers, interleukin- (IL-) 1β and IL-18, and inhibitors IL-1 receptor antagonist (IL-1Ra) and IL-18 binding protein (IL-18BP) were measured in plasma. Inflammasome activation was measured by caspase-1 enzymatic activity in monocytes in whole blood by flow cytometry, and expression of inflammasome-related genes was quantified using real-time PCR. Multiple linear regression analysis was used to investigate associations between PM exposures and inflammatory markers. Sex, age, smoking, current infection, BMI, and single nucleotide polymorphism in the inflammasome regulating genes CARD8 (C10X) and NLRP3 (Q705K) were included as covariates. 

    Results: The average exposure levels of respirable dust and quartz were 0.85 and 0.052 mg/m3, respectively. A significant exposure-response was found for respirable dust and IL-18 and for inhalable dust and IL-1Ra. Whole blood, drawn from study participants, was stimulated ex vivo with inflammasome priming stimuli LPS or Pam3CSK4, resulting in a 47% and 49% increase in caspase-1 enzymatic activity in monocytes. This increase in caspase-1 activity was significantly attenuated in the higher exposure groups for most PM exposure measures. 

    Conclusions: The results indicate that exposure levels of PM in the iron foundry environment can affect the NLRP3 inflammasome and systemic inflammation.

    Fulltekst (pdf)
    Quartz Dust Exposure Affects NLRP3 Inflammasome Activation and Plasma Levels of IL-18 and IL-1Ra in Iron Foundry Workers
  • 4.
    Kumawat, Ashok Kumar
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Nyhlin, Nils
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Wickbom, Anna
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Tysk, Curt
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Bohr, Johan
    Örebro universitet, Institutionen för hälsovetenskap och medicin. Region Örebro län. Department of Medicine, Division of Gastroenterology, Örebro University Hospital, Örebro, Sweden.
    Hultgren, Olof
    Department of Microbiology and Immunology, Örebro University Hospital, Örebro, Sweden.
    Hultgren-Hörnquist, Elisabeth
    Örebro universitet, Institutionen för läkarutbildning.
    An In Vitro Model to Evaluate the Impact of the Soluble Factors from the Colonic Mucosa of Collagenous Colitis Patients on T Cells: Enhanced Production of IL-17A and IL-10 from Peripheral CD4(+) T Cells2014Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikkel-id 879843Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Soluble factors from intestinal mucosal cells contribute to immune homeostasis in the gut. We have established an in vitro model to investigate the regulatory role of soluble factors from inflamed intestinal mucosa of collagenous colitis (CC) patients in the differentiation of T cells. Peripheral blood CD4(+) T cells from healthy donors were polyclonally activated in the presence of conditioned medium (CM) generated from denuded biopsies (DNB) or isolated lamina propria mononuclear cells (LPMCs) from mucosal biopsies from CC patients compared to noninflamed controls, to determine proliferation and secretion of cytokines involved in T-cell differentiation. Compared to controls, we observed significantly increased production of the proinflammatory cytokines IFN-gamma, IL-17A, IL-6, and IL-1 beta and the anti-inflammatory cytokines IL-4 and IL-10 in the presence of CC-DNB-CM. The most pronounced effect of CC-LPMC-CM on peripheral CD4(+) T cells was a trend towards increased production of IL-17A and IL-10. A trend towards reduced inhibition of T-cell proliferation was noted in the presence of CC-DNB-CM. In conclusion, our in vitro model reveals implications of soluble factors from CC colonic mucosa on peripheral T cells, enhancing their production of both pro-and anti-inflammatory cytokines.

  • 5.
    Paramel, Geena
    et al.
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Sirsjö, Allan
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Fransén, Karin
    Örebro universitet, Institutionen för hälsovetenskap och medicin.
    Role of genetic alterations in the NLRP3 and CARD8 genes in health and disease2015Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikkel-id 846782Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The complexity of a common inflammatory disease is influenced by multiple genetic and environmental factors contributing to the susceptibility of disease. Studies have reported that these exogenous and endogenous components may perturb the balance of innate immune response by activating the NLRP3 inflammasome. The multimeric NLRP3 complex results in the caspase-1 activation and the release of potent inflammatory cytokines, like IL-1β. Several studies have been performed on the association of the genetic alterations in genes encoding NLRP3 and CARD8 with the complex diseases with inflammatory background, like inflammatory bowel disease, cardiovascular diseases, rheumatoid arthritis, and type 1 diabetes. The aim of the present review is therefore to summarize the literature regarding genetic alterations in these genes and their association with health and disease.

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