BARRY COLE

Summary

Affiliation: University of Utah
Country: USA

Publications

  1. ncbi Allelic polymorphisms at the H-2A and HLA-DQ loci influence the response of murine lymphocytes to the Mycoplasma arthritidis superantigen MAM
    B C Cole
    Division of Rheumatology, University of Utah School of Medicine, Salt Lake City 84132, USA
    Infect Immun 65:4190-8. 1997
  2. ncbi Isolation and partial purification of macrophage- and dendritic cell-activating components from Mycoplasma arthritidis: association with organism virulence and involvement with Toll-like receptor 2
    Barry C Cole
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Infect Immun 73:6039-47. 2005
  3. ncbi Presence of Lps(d) mutation influences cytokine regulation in vivo by the Mycoplasma arthritidis mitogen superantigen and lethal toxicity in mice infected with M. arthritidis
    H H Mu
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132, USA
    Infect Immun 69:3837-44. 2001
  4. ncbi Engagement of Toll-like receptors by mycoplasmal superantigen: downregulation of TLR2 by MAM/TLR4 interaction
    H H Mu
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Cell Microbiol 7:789-97. 2005
  5. ncbi TLR2 and TLR4 differentially regulate B7-1 resulting in distinct cytokine responses to the mycoplasma superantigen MAM as well as to disease induced by Mycoplasma arthritidis
    Hong Hua Mu
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Cell Microbiol 8:414-26. 2006
  6. ncbi Inflammatory lipoproteins purified from a toxigenic and arthritogenic strain of Mycoplasma arthritidis are dependent on Toll-like receptor 2 and CD14
    Akira Hasebe
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Infect Immun 75:1820-6. 2007
  7. ncbi Characterization and partial purification of a macrophage-stimulating factor from Mycoplasma hominis
    Morgan R Peltier
    Department of Obstetrics, Gynecology and Reproductive Sciences, University of Medicine and Dentistry Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Am J Reprod Immunol 54:342-51. 2005
  8. ncbi A microbial TLR2 agonist imparts macrophage-activating ability to apolipoprotein A-1
    Akira Hasebe
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    J Immunol 177:4826-32. 2006
  9. ncbi Characterization of the macrophage-stimulating activity from Ureaplasma urealyticum
    Morgan R Peltier
    Department of Obstetrics, Gynecology and Reproductive Sciences, University of Medicine and Dentistry Robert Wood Johnson Medical School, 125 Patterson Street, New Brunswick, NJ 08901, USA
    Am J Reprod Immunol 57:186-92. 2007

Research Grants

  1. MYCOPLASMA-CELL INTERACTIONS AND INTERFERON INDUCTION
    BARRY COLE; Fiscal Year: 1980
  2. MYCOPLASMA SUPERANTIGEN MAM IN DISEASE AND AUTOIMMUNITY
    BARRY COLE; Fiscal Year: 2002
  3. MYCOPLASMA ARTHRITIDIS T CELL MITOGEN
    BARRY COLE; Fiscal Year: 1993
  4. MYCOPLASMA SUPERANTIGEN MAM IN DISEASE AND AUTOIMMUNITY
    BARRY COLE; Fiscal Year: 1993
  5. Mycoplasma Superantigen & RA MHC Susceptibility Alleles
    BARRY COLE; Fiscal Year: 2006

Collaborators

Detail Information

Publications9

  1. ncbi Allelic polymorphisms at the H-2A and HLA-DQ loci influence the response of murine lymphocytes to the Mycoplasma arthritidis superantigen MAM
    B C Cole
    Division of Rheumatology, University of Utah School of Medicine, Salt Lake City 84132, USA
    Infect Immun 65:4190-8. 1997
    ..Allelic polymorphisms at MHC loci might therefore influence susceptibility to autoimmune disease by affecting immunoreactivity to specific superantigens...
  2. ncbi Isolation and partial purification of macrophage- and dendritic cell-activating components from Mycoplasma arthritidis: association with organism virulence and involvement with Toll-like receptor 2
    Barry C Cole
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Infect Immun 73:6039-47. 2005
    ..Three active components were also found by reverse-phase chromatography. We suggest that macrophage activation by M. arthritidis could play a significant role in the inflammatory response induced in the host by this organism...
  3. ncbi Presence of Lps(d) mutation influences cytokine regulation in vivo by the Mycoplasma arthritidis mitogen superantigen and lethal toxicity in mice infected with M. arthritidis
    H H Mu
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City 84132, USA
    Infect Immun 69:3837-44. 2001
    ..arthritidis organisms. Our results suggest that MAM interacts with the lipopolysaccharide signaling pathway, possibly involving TLR4 or a combinatorial Toll complex...
  4. ncbi Engagement of Toll-like receptors by mycoplasmal superantigen: downregulation of TLR2 by MAM/TLR4 interaction
    H H Mu
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Cell Microbiol 7:789-97. 2005
    ..These results indicate that the SAg, MAM, interacts with both TLR2 and TLR4 and that TLR4 signalling might downregulate the MAM/TLR2 inflammatory response...
  5. ncbi TLR2 and TLR4 differentially regulate B7-1 resulting in distinct cytokine responses to the mycoplasma superantigen MAM as well as to disease induced by Mycoplasma arthritidis
    Hong Hua Mu
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Cell Microbiol 8:414-26. 2006
    ..Thus, TLR-mediated regulation of B7-1 results in diverse cytokine profiles in C3H sub-strains, and that the interaction of MAM with different TLR(s) may differentially affect cytokine responses and ultimately, M. arthritidis disease...
  6. ncbi Inflammatory lipoproteins purified from a toxigenic and arthritogenic strain of Mycoplasma arthritidis are dependent on Toll-like receptor 2 and CD14
    Akira Hasebe
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    Infect Immun 75:1820-6. 2007
    ..However, mass spectrometry of fragments revealed that the 41-kDa moiety, which binds to serum apolipoprotein A-1, had similarity with the recently described MlpD lipoprotein of M. arthritidis...
  7. ncbi Characterization and partial purification of a macrophage-stimulating factor from Mycoplasma hominis
    Morgan R Peltier
    Department of Obstetrics, Gynecology and Reproductive Sciences, University of Medicine and Dentistry Robert Wood Johnson Medical School, New Brunswick, NJ 08901, USA
    Am J Reprod Immunol 54:342-51. 2005
    ..The mechanism by which M. hominis, an organism lacking cell walls, increases the production of proinflammatory cytokines is unknown...
  8. ncbi A microbial TLR2 agonist imparts macrophage-activating ability to apolipoprotein A-1
    Akira Hasebe
    Division of Rheumatology, Department of Internal Medicine, University of Utah School of Medicine, 30 North 1900 East, Salt Lake City, UT 84132, USA
    J Immunol 177:4826-32. 2006
    ....
  9. ncbi Characterization of the macrophage-stimulating activity from Ureaplasma urealyticum
    Morgan R Peltier
    Department of Obstetrics, Gynecology and Reproductive Sciences, University of Medicine and Dentistry Robert Wood Johnson Medical School, 125 Patterson Street, New Brunswick, NJ 08901, USA
    Am J Reprod Immunol 57:186-92. 2007
    ..Therefore, we performed a series of experiments to understand better the bacterial factor(s) that are responsible for the proinflammatory effects of U. urealyticum...

Research Grants35

  1. MYCOPLASMA-CELL INTERACTIONS AND INTERFERON INDUCTION
    BARRY COLE; Fiscal Year: 1980
    ..The significance of interferon induction on the expression of mycoplasma-induced disease will also be evaluated...
  2. MYCOPLASMA SUPERANTIGEN MAM IN DISEASE AND AUTOIMMUNITY
    BARRY COLE; Fiscal Year: 2002
    ..Specifically the investigator shall define the role played by SAg-induced cytokines and protection against disease using the MAM vaccines described earlier. ..
  3. MYCOPLASMA ARTHRITIDIS T CELL MITOGEN
    BARRY COLE; Fiscal Year: 1993
    ....
  4. MYCOPLASMA SUPERANTIGEN MAM IN DISEASE AND AUTOIMMUNITY
    BARRY COLE; Fiscal Year: 1993
    ..arthritidis on the T cell repertoire; c. Is chronic arthritis due to a restricted V beta TCR-bearing T cell subset? d. Do MAM or other superantigens play a role in disease chronicity and disease flare ups?..
  5. Mycoplasma Superantigen & RA MHC Susceptibility Alleles
    BARRY COLE; Fiscal Year: 2006
    ..arthritidis in these "humanized" mice and determine strategies to overcome the effect of the superantigen MAM in initiating disease pathogenesis by modification of the cytokine milieu. ..