oru.sePublikasjoner
Endre søk
Begrens søket
1 - 7 of 7
RefereraExporteraLink til resultatlisten
Permanent link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Treff pr side
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Forfatter A-Ø
  • Forfatter Ø-A
  • Tittel A-Ø
  • Tittel Ø-A
  • Type publikasjon A-Ø
  • Type publikasjon Ø-A
  • Eldste først
  • Nyeste først
  • Skapad (Eldste først)
  • Skapad (Nyeste først)
  • Senast uppdaterad (Eldste først)
  • Senast uppdaterad (Nyeste først)
  • Disputationsdatum (tidligste først)
  • Disputationsdatum (siste først)
  • Standard (Relevans)
  • Forfatter A-Ø
  • Forfatter Ø-A
  • Tittel A-Ø
  • Tittel Ø-A
  • Type publikasjon A-Ø
  • Type publikasjon Ø-A
  • Eldste først
  • Nyeste først
  • Skapad (Eldste først)
  • Skapad (Nyeste først)
  • Senast uppdaterad (Eldste først)
  • Senast uppdaterad (Nyeste først)
  • Disputationsdatum (tidligste først)
  • Disputationsdatum (siste først)
Merk
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 1.
    El Marghani, Ahmed
    Örebro universitet, Institutionen för naturvetenskap.
    Cell signaling in inflammatory diseases and development of antiinflammatory drugs2008Licentiatavhandling, monografi (Annet vitenskapelig)
    Download (pdf)
    omslag
  • 2.
    El Marghani, Ahmed
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Regulatory aspects of innate immune responses2011Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Activation of innate immunity is regulated by a variety of signaling molecules within the immune cells. The present thesis was aimed to improve our understanding of innate signaling mechanism and their possible use as bio-indicators of exposure and disease. The first part of the thesis deals with the involvement of TOM1L1 (Target of Myb1 like 1) in innate immune signaling and regulation of inflammatory cytokines in immune cells (study I and II). The initial event of T-cells activation depend on the recruitment of Src family kinases Fyn and Lck, leading to interleukine-2 (IL-2) production in T cells. Understanding the regulatory aspects of IL-2 induction in T-cells is of importance as IL-2 is a key regulator for T-cell proliferation and survival. Interaction screening indicated the ability of TOM1L1 protein to interact with Fyn, and Lck, that is important for IL-2 production in Jurkat T-cells. TOM1L1 silencing decreased the levels of CD3/CD28 dependent induction of IL-2 in Jurkat T-cells, and LPS dependent induction of TNF-α in THP-1. Furthermore, overexpression of TOM1L1 in Jurkat T-cells causes an increase of STAT3 expression. This was accompanied by an increase in the levels of IL-1β dependent induction of IL-6 and TNF-α in THP-1 cells. These results indicate that TOM1L11 participate in regulation of innate immune response. The second part of the thesis deals with development of innate immune signaling responses used as a diagnosis tools for disease and exposure (study III and IV). Inflammatory diseases are associated with innate immune reactions. In response to inflammation, the immune cells release inflammatory cytokines such as IL-1-β, IL-2, IL-6, IL-10, TNF-α and CXCL8. These cytokines are regulated by stress related kinases include MAP kinase proteins such as ERK1-2, JNK, and MAPK p38, through activation of transcription factors AP-1, ATF-2, and NF-AT. In a clinical study, it was observed that activated MAPK p38 has a potential role in the regulation of IL-10 expression in intermittent claudication. However, expression of IL-10 and MAPK p38 was opposed in stable angina group. Therefore, targeting MAPK p38 in inflammatory disease such as cardiovascular diseases, diabetes, and rheumatoid arthritis might be useful in development of treatment strategies. Innate immune reactions can also be used to monitor stress related inflammatory responses following environmental exposure of immune cells. Inflammatory responses of exposure were studied by in vitro exposure to waters from sewage treatment works and recipient waters. The analysis shows that exposure to inland waters can result in activated immune responses and that these responses are both site dependent and vary over time.

    Delarbeid
    1. TOM1L is involved in a novel signaling pathway important for the IL-2 production in Jurkat T cells stimulated by CD3/CD28 CoLigation
    Åpne denne publikasjonen i ny fane eller vindu >>TOM1L is involved in a novel signaling pathway important for the IL-2 production in Jurkat T cells stimulated by CD3/CD28 CoLigation
    2009 (engelsk)Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, s. 416298-Artikkel i tidsskrift (Fagfellevurdert) Published
    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.

    sted, utgiver, år, opplag, sider
    Hindawi Publishing Corporation, 2009
    HSV kategori
    Forskningsprogram
    Biologi
    Identifikatorer
    urn:nbn:se:oru:diva-21385 (URN)10.1155/2009/416298 (DOI)000276144100001 ()2-s2.0-77949305423 (Scopus ID)
    Tilgjengelig fra: 2012-01-27 Laget: 2012-01-27 Sist oppdatert: 2017-12-08bibliografisk kontrollert
    2. Involvement of TOM1L1 in cytokine regulation in THP-1 cells
    Åpne denne publikasjonen i ny fane eller vindu >>Involvement of TOM1L1 in cytokine regulation in THP-1 cells
    (engelsk)Manuskript (preprint) (Annet vitenskapelig)
    HSV kategori
    Forskningsprogram
    Biologi
    Identifikatorer
    urn:nbn:se:oru:diva-21459 (URN)
    Tilgjengelig fra: 2012-02-02 Laget: 2012-02-02 Sist oppdatert: 2017-10-17bibliografisk kontrollert
    3. High MAPK p38 activity and low level of IL-10 in intermittent claudication as opposed to stable angina
    Åpne denne publikasjonen i ny fane eller vindu >>High MAPK p38 activity and low level of IL-10 in intermittent claudication as opposed to stable angina
    Vise andre…
    2010 (engelsk)Inngår i: International Journal of Angiology, ISSN 0392-9590, E-ISSN 1827-1839, Vol. 29, nr 4, s. 331-337Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    AIM:

    The aim of the present pilot study was to relate the activity of MAPK p38 with the levels of pro- and anti-inflammatory cytokines in a small cohort of patients with either stable angina (N=5) or intermittent claudication (N=5) compared to healthy controls (N=10).

    METHODS:

    The activity of MAPK p38 was determined in peripheral blood mononuclear cells, isolated from whole blood by western blot using phospho-specific anti-MAPK p38 antibodies. Cytokine levels of 11 pro- and anti-inflammatory cytokines were determined from the serum using flow cytometry.

    RESULTS:

    We found a significant elevation of the MAPK p38 activity in the intermittent claudication group (P=0.0027) compared with the healthy control group whereas the stable angina group showed similar MAPK p38 activity as the healthy control group. The IL-10 level in serum found in the stable angina group was significantly higher compared with both the healthy control group (P=0.0116) and the intermittent claudication group (P=0.0317).

    CONCLUSION:

    Our results imply that there is a casual relationship between increased levels of the anti-inflammatory cytokines IL-10 and IL-4 and the activity of the MAPK p38. Possibly has IL-10 a protective role that down-regulates the activity of MAPK p38 and thereby further inflammatory processes in stable angina patients.

    sted, utgiver, år, opplag, sider
    Torino: Minerva Medica, 2010
    Emneord
    p38 mitogen-activated protein kinases, Interleukin-10, Intermittent claudication
    HSV kategori
    Forskningsprogram
    Kardiologi
    Identifikatorer
    urn:nbn:se:oru:diva-12845 (URN)000283516700007 ()20671651 (PubMedID)
    Tilgjengelig fra: 2011-01-10 Laget: 2011-01-03 Sist oppdatert: 2017-12-11bibliografisk kontrollert
    4. Immune cell activation by sewage treatment plant effluents and inland waters in Sweden
    Åpne denne publikasjonen i ny fane eller vindu >>Immune cell activation by sewage treatment plant effluents and inland waters in Sweden
    (engelsk)Manuskript (preprint) (Annet vitenskapelig)
    HSV kategori
    Forskningsprogram
    Biologi
    Identifikatorer
    urn:nbn:se:oru:diva-21457 (URN)
    Tilgjengelig fra: 2012-02-02 Laget: 2012-02-02 Sist oppdatert: 2017-10-17bibliografisk kontrollert
    Download (pdf)
    omslag
    Download (pdf)
    spikblad
  • 3.
    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.

  • 4.
    El Marghani, Ahmed
    et al.
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Kjellén, Peter
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Olsson, Per-Erik
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Involvement of TOM1L1 in cytokine regulation in THP-1 cellsManuskript (preprint) (Annet vitenskapelig)
  • 5.
    El Marghani, Ahmed M.
    et al.
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Abuabaid, Hanan M.
    Örebro universitet, Hälsoakademin.
    Hurtig-Wennlöf, Anita
    Örebro universitet, Hälsoakademin.
    Sirsjö, Allan
    Örebro universitet, Hälsoakademin.
    Norgren, Lars
    Department of Surgery, Örebro University Hospital, Örebro, Sweden.
    Kjellén, Peter
    Örebro universitet, Akademin för naturvetenskap och teknik.
    High MAPK p38 activity and low level of IL-10 in intermittent claudication as opposed to stable angina2010Inngår i: International Journal of Angiology, ISSN 0392-9590, E-ISSN 1827-1839, Vol. 29, nr 4, s. 331-337Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    AIM:

    The aim of the present pilot study was to relate the activity of MAPK p38 with the levels of pro- and anti-inflammatory cytokines in a small cohort of patients with either stable angina (N=5) or intermittent claudication (N=5) compared to healthy controls (N=10).

    METHODS:

    The activity of MAPK p38 was determined in peripheral blood mononuclear cells, isolated from whole blood by western blot using phospho-specific anti-MAPK p38 antibodies. Cytokine levels of 11 pro- and anti-inflammatory cytokines were determined from the serum using flow cytometry.

    RESULTS:

    We found a significant elevation of the MAPK p38 activity in the intermittent claudication group (P=0.0027) compared with the healthy control group whereas the stable angina group showed similar MAPK p38 activity as the healthy control group. The IL-10 level in serum found in the stable angina group was significantly higher compared with both the healthy control group (P=0.0116) and the intermittent claudication group (P=0.0317).

    CONCLUSION:

    Our results imply that there is a casual relationship between increased levels of the anti-inflammatory cytokines IL-10 and IL-4 and the activity of the MAPK p38. Possibly has IL-10 a protective role that down-regulates the activity of MAPK p38 and thereby further inflammatory processes in stable angina patients.

  • 6.
    El Marghani, Ahmed M.
    et al.
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Khalaf, Hazem
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Jass, Jana
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Olsson, Per-Erik
    Örebro universitet, Akademin för naturvetenskap och teknik.
    Immune cell activation by sewage treatment plant effluents and inland waters in SwedenManuskript (preprint) (Annet vitenskapelig)
  • 7.
    Elmarghani, Ahmed
    et al.
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Pradhan, Ajay
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Seyoum, Asmerom
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Khalaf, Hazem
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Ros, Torbjön
    Pelagia Miljokonsult AB, Umeå, Sweden.
    Forsberg, Lars-Håkan
    Mälarenergi AB, Vasterås, Sweden.
    Nermark, Tomas
    Karlskoga Energi MO AB, Karlskoga, Sweden.
    Osterman, Lisa
    Skebäcks Reningsverk, Örebro, Sweden.
    Wiklund, Ulf
    Tyrens AB, Umeå, Sweden.
    Ivarsson, Per
    ALS Scandinavia AB, Täby, Sweden.
    Jass, Jana
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Olsson, Per-Erik
    Örebro universitet, Institutionen för naturvetenskap och teknik.
    Contribution of pharmaceuticals, fecal bacteria and endotoxin to the inflammatory responses to inland waters2014Inngår i: Science of the Total Environment, ISSN 0048-9697, E-ISSN 1879-1026, Vol. 488-489, s. 228-235Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The increasing contamination of freshwater with pharmaceuticals, surfactants, pesticides and other organic compounds are of major concern. As these contaminants are detected at trace levels in the environment it is important to determine if they elicit biological responses at the observed levels. In addition to chemical pollutants, there is also a concern for increasing levels of bacteria and other microorganisms in freshwater systems. In an earlier study, we observed the activation of inflammatory systems downstream of a wastewater treatment plant (WWTP) in southern Sweden. We also observed that the water contained unidentified components that were pro-inflammatory and potentiated the immune response in human urinary bladder epithelial cells. In order to determine if these effects were unique for the studied site or represent a common response in Swedish water, we have now performed a study on three WWTPs and their recipient waters in central Sweden. Analysis of immune responses in urinary bladder epithelial cells, monocyte-like cells and blood mononuclear cells confirm that these waters activate the immune system as well as induce pro-inflammatory responses. The results indicate that the cytokine profiles correlate to the endotoxin load of the waters rather than to the levels of pharmaceuticals or culturable bacteria load, suggesting that measurements of endotoxin levels and immune responses would be a valuable addition to the analysis of inland waters.

1 - 7 of 7
RefereraExporteraLink til resultatlisten
Permanent link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf