LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 68

Search options

  1. Article ; Online: Nitric oxide induces segregation of decay accelerating factor (DAF or CD55) from the membrane lipid-rafts and its internalization in human endometrial cells.

    Banadakoppa, Manu / Goluszko, Pawel / Liebenthal, Daniel / Yallampalli, Chandra

    Cell biology international

    2012  Volume 36, Issue 10, Page(s) 901–907

    Abstract: Recent studies suggest that DAF (decay accelerating factor), a complement regulatory protein, present in lipid rafts, is utilized by Dr fimbriated Escherichia coli for their binding and internalization. Previous studies in our laboratory have shown that ... ...

    Abstract Recent studies suggest that DAF (decay accelerating factor), a complement regulatory protein, present in lipid rafts, is utilized by Dr fimbriated Escherichia coli for their binding and internalization. Previous studies in our laboratory have shown that NO (nitric oxide) can reduce the invasion of Dr(+) E. coli and the severity of uterine infection in pregnant rats. Also, the expression level of DAF both at the mRNA and protein levels has been shown to be reduced by NO. Therefore NO mediated down-regulation of DAF appears to be an important factor in reducing the susceptibility to E. coli infection. However, it is unclear if NO can actually modulate the membrane association of DAF and therefore initial bacterial binding to cells. We found that NO induces the delocalization of DAF from the G(M1)-rich lipid rafts. Using biochemical and cell biological approaches in a uterine epithelial cell model (Ishikawa cells), DAF accumulates in caveolae upon exposure to NO. Interaction of DAF with the caveolar protein, caveolin1, leads to their internalization by endosomes. NO-induced delocalization of DAF from the lipid raft and its accumulation in caveolae are mediated through a cGMP (cyclic guanosine monophosphate) pathway. The acute localized synthesis of NO and its influence on DAF localization may represent an important unrecognized phenomenon of host defence against Dr(+) E. coli bacteria, as well as many disease conditions that involve complement system.
    MeSH term(s) CD55 Antigens/metabolism ; Caveolae/metabolism ; Caveolin 1/metabolism ; Cell Line ; Cyclic GMP/metabolism ; Endometrium/cytology ; Endometrium/microbiology ; Endosomes/metabolism ; Female ; Humans ; Nitric Oxide/metabolism
    Chemical Substances CD55 Antigens ; Caveolin 1 ; Nitric Oxide (31C4KY9ESH) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2012-05-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1143453-3
    ISSN 1095-8355 ; 1065-6995
    ISSN (online) 1095-8355
    ISSN 1065-6995
    DOI 10.1042/CBI20110586
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article: Membrane cholesterol: a crucial molecule affecting interactions of microbial pathogens with mammalian cells.

    Goluszko, P / Nowicki, B

    Infection and immunity

    2005  Volume 73, Issue 12, Page(s) 7791–7796

    MeSH term(s) Animals ; Bacteria/pathogenicity ; Cholesterol/analysis ; Cholesterol/metabolism ; Cholesterol/physiology ; Homeostasis ; Humans ; Infection/metabolism ; Infection/microbiology ; Membrane Microdomains/chemistry ; Membrane Microdomains/metabolism ; Membrane Microdomains/microbiology ; Viruses/metabolism ; Viruses/pathogenicity
    Chemical Substances Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2005-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.73.12.7791-7796.2005
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: Experimental autoimmune myasthenia gravis in the mouse.

    Wu, Bo / Goluszko, Elzbieta / Huda, Ruksana / Tüzün, Erdem / Christadoss, Premkumar

    Current protocols in immunology

    2013  Volume Chapter 15, Page(s) Unit 15.8.

    Abstract: Myasthenia gravis (MG) is a T cell-dependent antibody-mediated autoimmune neuromuscular disease. Antibodies to the nicotinic acetylcholine receptor (AChR) destroy the AChR, thus leading to defective neuromuscular transmission of electrical impulse and to ...

    Abstract Myasthenia gravis (MG) is a T cell-dependent antibody-mediated autoimmune neuromuscular disease. Antibodies to the nicotinic acetylcholine receptor (AChR) destroy the AChR, thus leading to defective neuromuscular transmission of electrical impulse and to muscle weakness. This unit is a practical guide to the induction and evaluation of experimental autoimmune myasthenia gravis (EAMG) in the mouse, the animal model for MG. Protocols are provided for the extraction and purification of AChR from the electric organs of Torpedo californica, or the electric ray. The purified receptor is used as an immunogen to induce autoimmunity to AChR, thus causing EAMG. The defect in neuromuscular transmission can also be measured quantitatively by electromyography. In addition, EAMG is frequently characterized by the presence of serum antibodies to AChR, which are measured by radioimmunoassay and by a marked antibody-mediated reduction in the number of muscle AChRs. AChR extracted from mouse muscle is used in measuring serum antibody levels and for quantifying muscle AChR content. Another hallmark of the disease is complement and IgG deposits located at the neuromuscular junction, which can be visualized by immunofluorescence techniques.
    MeSH term(s) Animals ; Autoantibodies/biosynthesis ; Autoantibodies/immunology ; Complement System Proteins/immunology ; Electromyography ; Female ; Fish Proteins/administration & dosage ; Fish Proteins/immunology ; Fish Proteins/isolation & purification ; Immunoglobulin G/immunology ; Male ; Mice ; Muscle, Skeletal/immunology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/physiopathology ; Myasthenia Gravis, Autoimmune, Experimental/immunology ; Myasthenia Gravis, Autoimmune, Experimental/metabolism ; Myasthenia Gravis, Autoimmune, Experimental/physiopathology ; Neuromuscular Junction/drug effects ; Neuromuscular Junction/physiopathology ; Radioimmunoassay ; Receptors, Nicotinic/administration & dosage ; Receptors, Nicotinic/immunology ; Receptors, Nicotinic/isolation & purification ; Synaptic Transmission/drug effects ; Torpedo/physiology
    Chemical Substances Autoantibodies ; Fish Proteins ; Immunoglobulin G ; Receptors, Nicotinic ; Complement System Proteins (9007-36-7)
    Language English
    Publishing date 2013
    Publishing country United States
    Document type Journal Article
    ISSN 1934-368X
    ISSN (online) 1934-368X
    DOI 10.1002/0471142735.im1508s100
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article: Membrane Cholesterol: a Crucial Molecule Affecting Interactions of Microbial Pathogens with Mammalian Cells

    Goluszko, P / Nowicki, B

    Infection and immunity. 2005 Dec., v. 73, no. 12

    2005  

    Language English
    Dates of publication 2005-12
    Size p. 7791-7796.
    Document type Article
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

  5. Article ; Online: Experimental autoimmune myasthenia gravis in the mouse.

    Wu, B / Goluszko, E / Christadoss, P

    Current protocols in immunology

    2008  Volume Chapter 15, Page(s) Unit 15.8

    Abstract: Myasthenia gravis (MG) is a T cell-dependent antibody-mediated autoimmune neuromuscular disease. Antibodies to the nicotinic acetylcholine receptor (AChR) destroy the AChR, thus leading to defective neuromuscular transmission of electrical impulse and to ...

    Abstract Myasthenia gravis (MG) is a T cell-dependent antibody-mediated autoimmune neuromuscular disease. Antibodies to the nicotinic acetylcholine receptor (AChR) destroy the AChR, thus leading to defective neuromuscular transmission of electrical impulse and to muscle weakness. This unit is a practical guide to the induction and evaluation of experimental autoimmune myasthenia gravis (EAMG) in the mouse, the animal model for MG. Protocols are provided for the extraction and purification of AChR from the electric organs of Torpedo californica, or eel. The purified receptor is used as an immunogen to induce autoimmunity to AChR, thus causing EAMG. The defect in neuromuscular transmission can also be measured quantitatively by electromyography, as described here. In addition, EAMG is frequently characterized by the presence of antibodies to AChR, which are measured by radioimmunoassay and by a marked antibody-mediated reduction in the number of muscle AChRs. AChR extracted from mouse muscle is used in measuring serum antibody levels and for quantifying muscle AChR content.
    MeSH term(s) Animals ; Antibodies/immunology ; Chromatography, Affinity/instrumentation ; Chromatography, Affinity/methods ; Disease Models, Animal ; Electromyography/instrumentation ; Electromyography/methods ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Myasthenia Gravis, Autoimmune, Experimental/immunology ; Neurotoxins/chemistry ; Radioimmunoassay/methods ; Receptors, Nicotinic/immunology ; Receptors, Nicotinic/isolation & purification ; Sepharose/chemistry
    Chemical Substances Antibodies ; Neurotoxins ; Receptors, Nicotinic ; Sepharose (9012-36-6)
    Language English
    Publishing date 2008-04-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2179059-0
    ISSN 1934-368X ; 1934-3671
    ISSN (online) 1934-368X
    ISSN 1934-3671
    DOI 10.1002/0471142735.im1508s21
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: PI3K/Akt pathway restricts epithelial adhesion of Dr + Escherichia coli by down-regulating the expression of decay accelerating factor.

    Banadakoppa, Manu / Goluszko, Pawel / Liebenthal, Daniel / Nowicki, Bogdan J / Nowicki, Stella / Yallampalli, Chandra

    Experimental biology and medicine (Maywood, N.J.)

    2014  Volume 239, Issue 5, Page(s) 581–594

    Abstract: The urogenital microbial infection in pregnancy is an important cause of maternal and neonatal morbidity and mortality. Uropathogenic Escherichia coli strains which express Dr fimbriae (Dr+) are associated with unique gestational virulence and they ... ...

    Abstract The urogenital microbial infection in pregnancy is an important cause of maternal and neonatal morbidity and mortality. Uropathogenic Escherichia coli strains which express Dr fimbriae (Dr+) are associated with unique gestational virulence and they utilize cell surface decay accelerating factor (DAF or CD55) as one of the cellular receptor before invading the epithelial cells. Previous studies in our laboratory established that nitric oxide reduces the rate of E. coli invasion by delocalizing the DAF protein from cell surface lipid rafts and down-regulating its expression. The phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) cell signal pathway plays an important role in host-microbe interaction because many bacteria including E. coli activate this pathway in order to establish infection. In the present study, we showed that the PI3K/Akt pathway negatively regulated the expression of DAF on the epithelial cell surface and thus inhibited the adhesion of Dr(+) E. coli to epithelial cells. Initially, using two human cell lines Ishikawa and HeLa which differ in constitutive activity of PI3K/Akt, we showed that DAF levels were associated with the PI3K/Akt pathway. We then showed that the DAF gene expression was up-regulated and the Dr(+) E. coli adhesion increased after the suppression of PI3K/Akt pathway in Ishikawa cells using inhibitor LY294002, and a plasmid which allowed the expression of PI3K/Akt regulatory protein PTEN. The down-regulation of PTEN protein using PTEN-specific siRNA activated the PI3K/Akt pathway, down-regulated the DAF, and decreased the adhesion of Dr(+) E. coli. We conclude that the PI3K/Akt pathway regulated the DAF expression in a nitric oxide independent manner.
    MeSH term(s) 3-Phosphoinositide-Dependent Protein Kinases/metabolism ; Adhesins, Escherichia coli/metabolism ; Bacterial Adhesion ; CD55 Antigens/biosynthesis ; Cell Line ; Down-Regulation ; Enzyme Inhibitors/metabolism ; Epithelial Cells/microbiology ; Epithelial Cells/physiology ; Female ; Gene Knockdown Techniques ; Humans ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; Uropathogenic Escherichia coli/physiology
    Chemical Substances Adhesins, Escherichia coli ; CD55 Antigens ; Dr adhesin, E coli ; Enzyme Inhibitors ; 3-Phosphoinositide-Dependent Protein Kinases (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2014-03-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 4015-0
    ISSN 1535-3699 ; 1525-1373 ; 0037-9727
    ISSN (online) 1535-3699 ; 1525-1373
    ISSN 0037-9727
    DOI 10.1177/1535370214522183
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Experimental autoimmune myasthenia gravis in the mouse.

    Wu, Bo / Goluszko, Elzbieta / Huda, Ruksana / Tüzün, Erdem / Christadoss, Premkumar

    Current protocols in immunology

    2011  Volume Chapter 15, Page(s) Unit 15.23

    Abstract: Myasthenia gravis (MG) is a T cell-dependent antibody-mediated autoimmune neuromuscular disease. Antibodies to the nicotinic acetylcholine receptor (AChR) destroy the AChR, thus leading to defective neuromuscular transmission of electrical impulse and to ...

    Abstract Myasthenia gravis (MG) is a T cell-dependent antibody-mediated autoimmune neuromuscular disease. Antibodies to the nicotinic acetylcholine receptor (AChR) destroy the AChR, thus leading to defective neuromuscular transmission of electrical impulse and to muscle weakness. This unit is a practical guide to the induction and evaluation of experimental autoimmune myasthenia gravis (EAMG) in the mouse, the animal model for MG. Protocols are provided for the extraction and purification of AChR from the electric organs of Torpedo californica, or the electric ray. The purified receptor is used as an immunogen to induce autoimmunity to AChR, thus causing EAMG. The defect in neuromuscular transmission can also be measured quantitatively by electromyography. In addition, EAMG is frequently characterized by the presence of serum antibodies to AChR, which are measured by radioimmunoassay and by a marked antibody-mediated reduction in the number of muscle AChRs. AChR extracted from mouse muscle is used in measuring serum antibody levels and for quantifying muscle AChR content. Another hallmark of the disease is complement and IgG deposits located at the neuromuscular junction, which can be visualized by immunofluorescence techniques.
    MeSH term(s) Animals ; Electric Organ/immunology ; Electromyography ; Immunoglobulin G/immunology ; Mice ; Mice, Inbred C57BL ; Muscle, Skeletal/immunology ; Myasthenia Gravis, Autoimmune, Experimental/immunology ; Neuromuscular Junction/immunology ; Receptors, Nicotinic/immunology ; Receptors, Nicotinic/isolation & purification ; Torpedo/immunology
    Chemical Substances Immunoglobulin G ; Receptors, Nicotinic
    Language English
    Publishing date 2011-11
    Publishing country United States
    Document type Journal Article
    ISSN 1934-368X
    ISSN (online) 1934-368X
    DOI 10.1002/0471142735.im1523s95
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Hemolityczne właściwości pałeczek Acinetobacter calcoaceticus.

    Gołuszko, P / Gospodarek, E

    Medycyna doswiadczalna i mikrobiologia

    1988  Volume 40, Issue 4, Page(s) 219–225

    Title translation Hemolytic properties of Acinetobacter calcoaceticus strains.
    MeSH term(s) Acinetobacter/physiology ; Animals ; Cattle ; Erythrocytes/physiology ; Hemolysis ; Horses ; Humans ; In Vitro Techniques ; Sheep
    Language Polish
    Publishing date 1988
    Publishing country Poland
    Document type Comparative Study ; English Abstract ; Journal Article
    ZDB-ID 411641-0
    ISSN 0025-8601 ; 0465-5893 ; 0368-9158
    ISSN 0025-8601 ; 0465-5893 ; 0368-9158
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article: Treatment of experimental autoimmune myasthenia gravis with recombinant human tumor necrosis factor receptor Fc protein.

    Christadoss, Premkumar / Goluszko, Elzbieta

    Journal of neuroimmunology

    2001  Volume 122, Issue 1-2, Page(s) 186–190

    Abstract: Lymphotoxin-alpha (TNF-beta) and TNF receptor p55 gene knockout mice are resistant to the development of antibody and complement mediated experimental autoimmune myasthenia gravis (EAMG), suggesting a possible role of TNF in mediating EAMG. Therefore, we ...

    Abstract Lymphotoxin-alpha (TNF-beta) and TNF receptor p55 gene knockout mice are resistant to the development of antibody and complement mediated experimental autoimmune myasthenia gravis (EAMG), suggesting a possible role of TNF in mediating EAMG. Therefore, we tested the hypothesis that blocking the functional interaction of TNF with their receptors by soluble recombinant human TNFR:Fc would suppress the ongoing clinical EAMG. Recombinant human TNFR:Fc administered daily for 2 weeks to C57BL6 mice with ongoing clinical EAMG significantly improved clinical EAMG when compared with placebo-treated mice. A clinical trial of selected myasthenia gravis patients with recombinant human TNFR:Fc could be attempted.
    MeSH term(s) Animals ; Antigens, CD/genetics ; Etanercept ; Immunoglobulin G/pharmacology ; Immunosuppressive Agents/pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myasthenia Gravis, Autoimmune, Experimental/drug therapy ; Receptors, Tumor Necrosis Factor/genetics ; Receptors, Tumor Necrosis Factor, Type I
    Chemical Substances Antigens, CD ; Immunoglobulin G ; Immunosuppressive Agents ; Receptors, Tumor Necrosis Factor ; Receptors, Tumor Necrosis Factor, Type I ; Etanercept (OP401G7OJC)
    Language English
    Publishing date 2001-12-14
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 8335-5
    ISSN 1872-8421 ; 0165-5728
    ISSN (online) 1872-8421
    ISSN 0165-5728
    DOI 10.1016/s0165-5728(01)00473-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article: Vaccination with purified Dr Fimbriae reduces mortality associated with chronic urinary tract infection due to Escherichia coli bearing Dr adhesin.

    Goluszko, Pawel / Goluszko, Elzbieta / Nowicki, Bogdan / Nowicki, Stella / Popov, Vsevolod / Wang, Hui-Qun

    Infection and immunity

    2004  Volume 73, Issue 1, Page(s) 627–631

    Abstract: The vaccination of C3H/HeJ mice with Escherichia coli Dr fimbrial antigen reduced mortality associated with an experimental urinary tract infection due to a homologous strain bearing Dr adhesin. Immune sera with high titers of anti-Dr antibody inhibited ... ...

    Abstract The vaccination of C3H/HeJ mice with Escherichia coli Dr fimbrial antigen reduced mortality associated with an experimental urinary tract infection due to a homologous strain bearing Dr adhesin. Immune sera with high titers of anti-Dr antibody inhibited bacterial binding to bladders and kidneys but did not affect the rate of renal colonization.
    MeSH term(s) Adhesins, Escherichia coli/physiology ; Animals ; Chronic Disease ; Escherichia coli Infections/prevention & control ; Escherichia coli Proteins/immunology ; Female ; Fimbriae Proteins/immunology ; Mice ; Mice, Inbred C3H ; Urinary Tract Infections/prevention & control ; Vaccination
    Chemical Substances Adhesins, Escherichia coli ; Escherichia coli Proteins ; Fimbriae Proteins (147680-16-8)
    Language English
    Publishing date 2004-12-21
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 218698-6
    ISSN 1098-5522 ; 0019-9567
    ISSN (online) 1098-5522
    ISSN 0019-9567
    DOI 10.1128/IAI.73.1.627-631.2005
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top