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Elmarghani, Ahmed
Alternative names
Publications (7 of 7) Show all publications
Elmarghani, A., Pradhan, A., Seyoum, A., Khalaf, H., Ros, T., Forsberg, L.-H., . . . Olsson, P.-E. (2014). Contribution of pharmaceuticals, fecal bacteria and endotoxin to the inflammatory responses to inland waters. Science of the Total Environment, 488-489, 228-235
Open this publication in new window or tab >>Contribution of pharmaceuticals, fecal bacteria and endotoxin to the inflammatory responses to inland waters
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2014 (English)In: Science of the Total Environment, ISSN 0048-9697, E-ISSN 1879-1026, Vol. 488-489, p. 228-235Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Wastewater treatment plants; Immune response; Cytokines; Bacteria; Inflammation; Pharmaceuticals
National Category
Environmental Sciences
Research subject
Enviromental Science
Identifiers
urn:nbn:se:oru:diva-35474 (URN)10.1016/j.scitotenv.2014.04.090 (DOI)000338600800023 ()24836131 (PubMedID)2-s2.0-84900490429 (Scopus ID)
Funder
Knowledge Foundation
Note

Funding Agencies:

City of Örebro

Karlskoga Energi och Miljö AB

Mälarenergi AB

Pelagia Miljökonsult AB

Tyrens AB

Örebro University

Available from: 2014-06-24 Created: 2014-06-24 Last updated: 2019-01-10Bibliographically approved
El Marghani, A. (2011). Regulatory aspects of innate immune responses. (Doctoral dissertation). Örebro: Örebro universitet
Open this publication in new window or tab >>Regulatory aspects of innate immune responses
2011 (English)Doctoral thesis, comprehensive summary (Other academic)
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.

Place, publisher, year, edition, pages
Örebro: Örebro universitet, 2011. p. 56
Series
Örebro Studies in Life Science ; 9
Keywords
Innate immunity, TOM1L1, inflammatory responses
National Category
Natural Sciences Biological Sciences
Research subject
Biology
Identifiers
urn:nbn:se:oru:diva-21384 (URN)978-91-7668-816-8 (ISBN)
Public defence
2011-10-31, Musikhögskolan, hörsal M, Fakultetsgatan 1, Örebro, 10:00 (English)
Opponent
Supervisors
Available from: 2012-01-30 Created: 2012-01-27 Last updated: 2017-10-17Bibliographically approved
El Marghani, A. M., Abuabaid, H. M., Hurtig-Wennlöf, A., Sirsjö, A., Norgren, L. & Kjellén, P. (2010). High MAPK p38 activity and low level of IL-10 in intermittent claudication as opposed to stable angina. International Journal of Angiology, 29(4), 331-337
Open this publication in new window or tab >>High MAPK p38 activity and low level of IL-10 in intermittent claudication as opposed to stable angina
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2010 (English)In: International Journal of Angiology, ISSN 0392-9590, E-ISSN 1827-1839, Vol. 29, no 4, p. 331-337Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
Torino: Minerva Medica, 2010
Keywords
p38 mitogen-activated protein kinases, Interleukin-10, Intermittent claudication
National Category
Medical and Health Sciences Cardiac and Cardiovascular Systems
Research subject
Cardiology
Identifiers
urn:nbn:se:oru:diva-12845 (URN)000283516700007 ()20671651 (PubMedID)
Available from: 2011-01-10 Created: 2011-01-03 Last updated: 2017-12-11Bibliographically approved
El Marghani, A., Abuabaid, H. & Kjellén, P. (2009). TOM1L is involved in a novel signaling pathway important for the IL-2 production in Jurkat T cells stimulated by CD3/CD28 CoLigation. Mediators of Inflammation, 416298
Open this publication in new window or tab >>TOM1L is involved in a novel signaling pathway important for the IL-2 production in Jurkat T cells stimulated by CD3/CD28 CoLigation
2009 (English)In: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, p. 416298-Article in journal (Refereed) 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.

Place, publisher, year, edition, pages
Hindawi Publishing Corporation, 2009
National Category
Biological Sciences
Research subject
Biology
Identifiers
urn:nbn:se:oru:diva-21385 (URN)10.1155/2009/416298 (DOI)000276144100001 ()2-s2.0-77949305423 (Scopus ID)
Available from: 2012-01-27 Created: 2012-01-27 Last updated: 2017-12-08Bibliographically approved
El Marghani, A. (2008). Cell signaling in inflammatory diseases and development of antiinflammatory drugs. (Licentiate dissertation). Örebro: Örebro universitet
Open this publication in new window or tab >>Cell signaling in inflammatory diseases and development of antiinflammatory drugs
2008 (English)Licentiate thesis, monograph (Other academic)
Place, publisher, year, edition, pages
Örebro: Örebro universitet, 2008. p. 53
Keywords
Cell signaling, antiinflammatory drugs, inflammatory diseases
National Category
Immunology in the medical area
Research subject
Immunology
Identifiers
urn:nbn:se:oru:diva-3712 (URN)
Presentation
(English)
Available from: 2008-12-29 Created: 2008-12-29 Last updated: 2018-01-13
El Marghani, A. M., Khalaf, H., Jass, J. & Olsson, P.-E.Immune cell activation by sewage treatment plant effluents and inland waters in Sweden.
Open this publication in new window or tab >>Immune cell activation by sewage treatment plant effluents and inland waters in Sweden
(English)Manuscript (preprint) (Other academic)
National Category
Biological Sciences
Research subject
Biology
Identifiers
urn:nbn:se:oru:diva-21457 (URN)
Available from: 2012-02-02 Created: 2012-02-02 Last updated: 2017-10-17Bibliographically approved
El Marghani, A., Kjellén, P. & Olsson, P.-E.Involvement of TOM1L1 in cytokine regulation in THP-1 cells.
Open this publication in new window or tab >>Involvement of TOM1L1 in cytokine regulation in THP-1 cells
(English)Manuscript (preprint) (Other academic)
National Category
Biological Sciences
Research subject
Biology
Identifiers
urn:nbn:se:oru:diva-21459 (URN)
Available from: 2012-02-02 Created: 2012-02-02 Last updated: 2017-10-17Bibliographically approved
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