Högskolan i Skövde

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  • 1.
    Ali, Abukar
    University of Skövde, School of Life Sciences.
    Time window of TNF-a in innate immunity against staphylococcal infection2010Independent thesis Basic level (degree of Bachelor), 20 credits / 30 HE creditsStudent thesis
    Abstract [en]

    Staphylococcus aureus (S. aureus) is responsible for many human diseases including septic arthritis and sepsis shock. Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine involved in inflammation and produced mainly by macrophages and monocytes. It is believed to be involved in pathogenesis of septic arthritis. Time window of TNF-a in innate immunity against staphylococcal infection was studied in this project.

    Two experiments were carried out: In the first experiment mice were infected with a low dose (8x106cfu/mouse) of S. aureus to induce septic arthritis whereas in the second experiment the mice were infected with a higher dose (8x107cfu/mouse) of S. aureus to induce sepsis shock. All mice were divided into three groups. The first group was treated with anti-TNF-α 20 minutes after infection. The second group was treated with the anti-TNF-α three days after infection. The third group served as control and was injected with PBS instead of anti-TNF-α. The mice were regularly weighed and signs of arthritis and mortality were recorded. Two weeks after inoculation bacteria viable counts in different organs was done, as well as histopathological assessment of joints and measurement of cytokines in blood.

    We have observed that mice treated with anti-TNF-α had less severe arthritis and also less mortality. However, they had more bacteria accumulated in the kidneys and lost more weight compared to the control group. The results were mostly seen in the group early treated with TNF-α, compared to the late treated group.

    We conclude that anti-TNF-α might be potentially used as a therapy against septic arthritis and sepsis shock. This should be combined with antibiotics to eliminate the bacteria while the anti-TNF-α reduces the severity of the inflammation and thus reduce the risk of permanent joint destruction and mortality. We can conclude that blocking TNF-α early on is essential in order to get the best results.

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  • 2.
    Celik, Yeliz
    et al.
    Department of Pulmonary Medicine, Koc University School of Medicine, Koc University Research Center for Translational Medicine (KUTTAM), Koc University, Istanbul, Turkey.
    Peker, Yüksel
    Department of Pulmonary Medicine, Koc University School of Medicine, Koc University Research Center for Translational Medicine (KUTTAM), Koc University, Istanbul, Turkey ; Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Sweden ; Department of Clinical Sciences, Respiratory Medicine and Allergology, Faculty of Medicine, Lund University, Sweden ; Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States ; Division of Sleep and Circadian Disorders, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, United States.
    Yucel-Lindberg, Tülay
    Department of Dental Medicine, Karolinska Institute, Stockholm, Sweden.
    Thelander, Tilia
    University of Skövde, School of Health Sciences. University of Skövde, Digital Health Research (DHEAR).
    Behboudi, Afrouz
    University of Skövde, School of Health Sciences. University of Skövde, Digital Health Research (DHEAR).
    Association of TNF-α (-308G/A) Gene Polymorphism with Changes in Circulating TNF-α Levels in Response to CPAP Treatment in Adults with Coronary Artery Disease and Obstructive Sleep Apnea2023In: Journal of Clinical Medicine, E-ISSN 2077-0383, Vol. 12, no 16, article id 5325Article in journal (Refereed)
    Abstract [en]

    Rationale: We recently demonstrated that patients with coronary artery disease (CAD) and obstructive sleep apnea (OSA) carrying the tumor necrosis factor-alpha (TNF-α) A allele had increased circulating TNF-α levels compared with the ones carrying the TNF-α G allele. In the current study, we addressed the effect of TNF-α (-308G/A) gene polymorphism on circulating TNF-α levels following continuous positive airway pressure (CPAP) therapy. Methods: This study was a secondary analysis of the RICCADSA trial (NCT00519597) conducted in Sweden. CAD patients with OSA (apnea–hypopnea index) of ≥15 events/h and an Epworth Sleepiness Scale (ESS) score of <10 were randomized to CPAP or no-CPAP groups, and OSA patients with an ESS score of ≥10 were offered CPAP treatment. Blood samples were obtained at baseline and 12-month follow-up visits. TNF-α was measured by immunoassay (Luminex, R&D Systems). Genotyping of TNF-α-308G/A (single nucleotide polymorphism Rs1800629) was performed by polymerase chain reaction–restriction fragment length polymorphism. Results: In all, 239 participants (206 men and 33 women; mean age 64.9 (SD 7.7) years) with polymorphism data and circulating levels of TNF-α at baseline and 1-year follow-up visits were included. The median circulating TNF-α values fell in both groups between baseline and 12 months with no significant within- or between-group differences. In a multivariate linear regression model, a significant change in circulating TNF-α levels from baseline across the genotypes from GA to GA and GA to AA (standardized β-coefficient −0.129, 95% confidence interval (CI) −1.82; −0.12; p = 0.025) was observed in the entire cohort. The association was more pronounced among the individuals who were using the device for at least 4 h/night (n = 86; standardized β-coefficient −2.979 (95% CI −6.11; −1.21); p = 0.004)), whereas no significant association was found among the patients who were non-adherent or randomized to no-CPAP. The participants carrying the TNF-α A allele were less responsive to CPAP treatment regarding the decline in circulating TNF-α despite CPAP adherence (standardized β-coefficient −0.212, (95% CI −5.66; −1.01); p = 0.005). Conclusions: Our results suggest that TNF-α (-308G/A) gene polymorphism is associated with changes in circulating TNF-α levels in response to CPAP treatment in adults with CAD and OSA. 

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  • 3.
    Jensen, Poul Erik H.
    et al.
    Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmar.
    Warnke, Clemens
    Department of Neurology, University Hospital Köln, Germany / University of Düsseldorf, Medical Faculty, Department of Neurology, Germany.
    Ingenhoven, Kathleen
    University of Düsseldorf, Medical Faculty, Department of Neurology, Germany.
    Piccoli, Luca
    Università della Svizzera italiana (USI), Faculty of Biomedical Sciences, Institute for Research in Biomedicine, Bellinzona, Switzerland.
    Gasis, Marcia
    University of Düsseldorf, Medical Faculty, Department of Neurology, Germany.
    Hermanrud, Christina
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Fernandez-Rodriguez, Blanca M.
    Università della Svizzera italiana (USI), Faculty of Biomedical Sciences, Institute for Research in Biomedicine, Bellinzona, Switzerland.
    Ryner, Malin
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Kramer, Daniel
    Sanofi-Aventis Germany, Frankfurt Am Main, Germany.
    Link, Jenny
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Ramanujam, Ryan
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden / KTH – Royal Institute of Technology, Stockholm, Sweden.
    Auer, Michael
    Innsbruck Medical University, Innsbruck, Austria.
    Buck, Dorothea
    Department of Neurology, Technische Universität München, Munich, Germany.
    Grummel, Verena
    Department of Neurology, Technische Universität München, Munich, Germany.
    Bertotti, Elisa
    Merck NBE Bioanalytics Ivrea, Colleretto Giacosa, Italy.
    Fissolo, Nicolas
    Hospital Universitari Vall d'Hebron, Centre d'Esclerosi Múltiple de Catalunya, Barcelona, Spain.
    Oliver-Martos, Begoña
    Hospital Regional Universitario de Málaga, Instituto de investigación Biomédica de Málaga (IBIMA), Universidad de Málaga, Spain.
    Nytrova, Petra
    MS Center, Department of Neurology and Center Clinical Neuroscience, Charles University in Prague, 1st Faculty of Medicine and General University Hospital, Prague, Czech Republic.
    Khalil, Michael
    Department of Neurology, Medical University of Graz, Austria.
    Guger, Michael
    Clinic for Neurology 2, Kepler University Clinic, Med Campus III, Linz, Austria.
    Rathmaier, Sandra
    Clinic for Neurology 2, Kepler University Clinic, Med Campus III, Linz, Austria.
    Sievers-Stober, Claudia
    Departments of Biomedicine and Neurology, University Hospital Basel and University of Basel, Switzerland.
    Lindberg, Raija L. P.
    Departments of Biomedicine and Neurology, University Hospital Basel and University of Basel, Switzerland.
    Hässler, Signe
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, Paris-Saclay, University UVSQ, Villejuif, France.
    Bachelet, Delphine
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, Paris-Saclay, University UVSQ, Villejuif, France.
    Aktas, Orhan
    University of Düsseldorf, Medical Faculty, Department of Neurology, Germany.
    Donnellan, Naoimh
    Ipsen Biopharm Ltd., Berkshire, United Kingdom.
    Lawton, Andy
    GlaxoSmithKline R&D, Uxbridge, Middlesex, United Kingdom.
    Hemmer, Bernhard
    Department of Neurology, Technische Universität München, Germany / Munich Cluster for systems Neurology (SyNergy), Germany.
    Havrdova, Eva Kubala
    MS Center, Department of Neurology and Center Clinical Neuroscience, Charles University in Prague, 1st Faculty of Medicine and General University Hospital, Prague, Czech Republic.
    Kieseier, Bernd
    University of Düsseldorf, Medical Faculty, Department of Neurology, Germany.
    Hartung, Hans-Peter
    University of Düsseldorf, Medical Faculty, Department of Neurology, Germany.
    Comabella, Manuel
    Hospital Universitari Vall d'Hebron, Centre d'Esclerosi Múltiple de Catalunya, Barcelona, Spain.
    Montalban, Xavier
    Hospital Universitari Vall d'Hebron, Centre d'Esclerosi Múltiple de Catalunya, Barcelona, Spain.
    Derfuss, Tobias
    Departments of Biomedicine and Neurology, University Hospital Basel and University of Basel, Switzerland.
    Sellebjerg, Finn
    Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark.
    Dönnes, Pierre
    SciCross AB, Skövde, Sweden.
    Pallardy, Marc
    INSERM UMR 996, Univ. Paris-Sud, Faculty of Pharmacy, Université Paris-Saclay, Châtenay-Malabry, France.
    Spindeldreher, Sebastian
    Drug Metabolism Pharmacokinetics-Biologics, Novartis Institutes for Biomedical Research, Basel, Switzerland.
    Broët, Philippe
    CESP, INSERM UMR 1018, Faculty of Medicine, Paris-Sud University, Paris-Saclay, University UVSQ, Villejuif, France / Assistance Publique - Hôpitaux de Paris, Hôpital Paul Brousse, Villejuif, France.
    Deisenhammer, Florian
    Innsbruck Medical University, Austria.
    Fogdell-Hahn, Anna
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Sorensen, Per Soelberg
    Danish Multiple Sclerosis Center, Department of Neurology, Rigshospitalet, University of Copenhagen, Denmark.
    Detection and kinetics of persistent neutralizing anti-interferon-beta antibodies in patients with multiple sclerosis: Results from the ABIRISK prospective cohort study2019In: Journal of Neuroimmunology, ISSN 0165-5728, E-ISSN 1872-8421, Vol. 326, p. 19-27Article in journal (Refereed)
    Abstract [en]

    Two validated assays, a bridging ELISA and a luciferase-based bioassay, were compared for detection of anti-drug antibodies (ADA) against interferon-beta (IFN-β) in patients with multiple sclerosis. Serum samples were tested from patients enrolled in a prospective study of 18 months. In contrast to the ELISA, when IFN-β-specific rabbit polyclonal and human monoclonal antibodies were tested, the bioassay was the more sensitive to detect IFN-β ADA in patients' sera. For clinical samples, selection of method of ELISA should be evaluated prior to the use of a multi-tiered approach. A titer threshold value is reported that may be used as a predictor for persistently positive neutralizing ADA.

  • 4.
    Sundell, Timothy
    et al.
    Department of Rheumatology and Inflammation Research, University of Gothenburg, Sweden.
    Grimstad, Kristoffer
    University of Skövde, School of Bioscience. University of Skövde, Systems Biology Research Environment. Department of Rheumatology and Inflammation Research, University of Gothenburg, Sweden.
    Camponeschi, Alessandro
    Department of Rheumatology and Inflammation Research, University of Gothenburg, Sweden.
    Tilevik, Andreas
    University of Skövde, School of Bioscience. University of Skövde, Systems Biology Research Environment.
    Gjertsson, Inger
    Department of Rheumatology and Inflammation Research, University of Gothenburg, Sweden.
    Mårtensson, Inga-Lill
    Department of Rheumatology and Inflammation Research, University of Gothenburg, Sweden.
    Single-cell RNA sequencing analyses: interference by the genes that encode the B-cell and T-cell receptors2023In: Briefings in Functional Genomics & Proteomics, ISSN 2041-2649, E-ISSN 2041-2657, Vol. 22, no 3, p. 263-273, article id elac044Article in journal (Refereed)
    Abstract [en]

    B and T cells are integral parts of the immune system and are implicated in many diseases, e.g. autoimmunity. Towards understanding the biology of B and T cells and subsets thereof, their transcriptomes can be analyzed using single-cell RNA sequencing. In some studies, the V(D)J transcripts encoding the variable regions of the B- and T-cell antigen receptors have been removed before the analyses. However, a systematic analysis of the effects of including versus excluding these genes is currently lacking. We have investigated the effects of these transcripts on unsupervised clustering and down-stream analyses of single-cell RNA sequencing data from B and T cells. We found that exclusion of the B-/T-cell receptor genes prior to unsupervised clustering resulted in clusters that represented biologically meaningful subsets, such as subsets of memory B and memory T cells. Furthermore, pseudo-time and trajectory inference analyses of early B-lineage cells resulted in a developmental pathway from progenitor to immature B cells. In contrast, when the B-/T-cell receptor genes were not removed, with the PCs used for clustering consisting of up to 70% V-genes, this resulted in some clusters being defined exclusively by V-gene segments. These did not represent biologically meaningful subsets; for instance in the early B-lineage cells, these clusters contained cells representing all developmental stages. Thus, in studies of B and T cells, to derive biologically meaningful results, it is imperative to remove the gene sequences that encode B- and T-cell receptors.

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  • 5.
    Åkesson, Julia
    et al.
    University of Skövde, School of Bioscience. University of Skövde, Systems Biology Research Environment. Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Sweden.
    Hojjati, Sara
    Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Hellberg, Sandra
    Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Sweden ; Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Raffetseder, Johanna
    Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Khademi, Mohsen
    Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Rynkowski, Robert
    Department of Neurology, and Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Kockum, Ingrid
    Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Altafini, Claudio
    Division of Automatic Control, Department of Electrical Engineering, Linköping University, Sweden.
    Lubovac-Pilav, Zelmina
    University of Skövde, School of Bioscience. University of Skövde, Systems Biology Research Environment.
    Mellergård, Johan
    Department of Neurology, and Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Jenmalm, Maria C.
    Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Piehl, Fredrik
    Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Olsson, Tomas
    Neuroimmunology Unit, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden.
    Ernerudh, Jan
    Department of Clinical Immunology and Transfusion Medicine, and Department of Biomedical and Clinical Sciences, Linköping University, Sweden.
    Gustafsson, Mika
    Bioinformatics, Department of Physics, Chemistry and Biology, Linköping University, Sweden.
    Proteomics reveal biomarkers for diagnosis, disease activity and long-term disability outcomes in multiple sclerosis2023In: Nature Communications, E-ISSN 2041-1723, Vol. 14, no 1, article id 6903Article in journal (Refereed)
    Abstract [en]

    Sensitive and reliable protein biomarkers are needed to predict disease trajectory and personalize treatment strategies for multiple sclerosis (MS). Here, we use the highly sensitive proximity-extension assay combined with next-generation sequencing (Olink Explore) to quantify 1463 proteins in cerebrospinal fluid (CSF) and plasma from 143 people with early-stage MS and 43 healthy controls. With longitudinally followed discovery and replication cohorts, we identify CSF proteins that consistently predicted both short- and long-term disease progression. Lower levels of neurofilament light chain (NfL) in CSF is superior in predicting the absence of disease activity two years after sampling (replication AUC = 0.77) compared to all other tested proteins. Importantly, we also identify a combination of 11 CSF proteins (CXCL13, LTA, FCN2, ICAM3, LY9, SLAMF7, TYMP, CHI3L1, FYB1, TNFRSF1B and NfL) that predict the severity of disability worsening according to the normalized age-related MS severity score (replication AUC = 0.90). The identification of these proteins may help elucidate pathogenetic processes and might aid decisions on treatment strategies for persons with MS.

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