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Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes

  1. Author:
    Cabral, E. S.
    Gelderblom, H.
    Hornung, R. L.
    Munson, P. J.
    Martin, R.
    Marques, A. R.

  2. Author Address

    NIAID, Clin Studies Unit, Lab Clin Infect Dis, NIH, Bethesda, MD 20892 USA. NINDS, Cellular Immunol Sect, Neuroimmunol Branch, Bethesda, MD 20892 USA. NIH, Math & Stat Comp Lab, Div Computat Biosci, Ctr Informat Technol, Bethesda, MD 20892 USA. SAIC Frederick Inc, Clin Serv Program, NCI Frederick, Frederick, MD USA.;Marques, AR, NIAID, Clin Studies Unit, Lab Clin Infect Dis, NIH, Bldg 10 Rm 11N228,10 Ctr Dr, Bethesda, MD 20892 USA.;amarques@niaid.nih.gov
    1. Year: 2006
    2. Date: Mar
  2. Journal: Journal of Infectious Diseases
    1. 193
    2. 6
    3. Pages: 849-859
  4. Type of Article: Article
  5. ISSN: 0022-1899
  1. Abstract:

    Toll-like receptors (TLRs) trigger innate immune responses via the recognition of conserved pathogen-associated molecular patterns. Lipoproteins from Borrelia burgdorferi, the agent of Lyme disease, activate inflammatory cells through TLR2 and TLR1. We show that stimulation of human monocytes with B. burgdorferi lysate, lipidated outer surface protein A, and triacylated lipopeptide Pam(3)CysSerLys(4) results in the up-regulation of both TLR2 and TLR1 but the down-regulation of TLR5,the receptor for bacterial flagellin, and that this effect is mediated via TLR2. TLR4 stimulation had no effect on TLR2, TLR1, and TLR5 expression. Human monocytes stimulated with TLR5 ligands (including p37 or flaA, the minor protein from B. burgdorferi flagella) up-regulated TLR5. In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist. These results indicate that diverse stimuli can cause differential TLR expression, and we hypothesize that these changes may be useful for either the pathogen and/or the host.

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External Sources

  1. View record in Web of Science®
  2. WOS: 000235536200016

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