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Painful Pathways Induced by TLR Stimulation of Dorsal Root Ganglion Neurons

  1. Author:
    Qi, J.
    Buzas, K.
    Fan, H. T.
    Cohen, J. I.
    Wang, K. N.
    Mont, E.
    Klinman, D.
    Oppenheim, J. J.
    Howard, O. M. Z.

  2. Author Address

    [Qi, J; Buzas, K; Fan, HT; Oppenheim, JJ; Howard, OMZ] NCI, Mol Immunoregulat Lab, Canc & Inflammatory Program, Ctr Canc Res, Frederick, MD 21702 USA [Cohen, JI; Wang, KN] NIAID, Infect Dis Lab, NIH, Bethesda, MD 20892 USA [Mont, E] Nova Scotia Med Examiner Serv, Halifax, NS B3J1H6, Canada [Klinman, D] NCI, Expt Immunol Lab, Canc & Inflammatory Program, Ctr Canc Res, Frederick, MD 21702 USA;Howard, OMZ (reprint author), NCI, Mol Immunoregulat Lab, Canc & Inflammatory Program, Ctr Canc Res, POB B,1050 Boyles St, Frederick, MD 21702 USA;howardz@mail.nih.gov
    1. Year: 2011
    2. Date: Jun
  2. Journal: Journal of Immunology
    1. 186
    2. 11
    3. Pages: 6417-6426
  4. Type of Article: Article
  5. ISSN: 0022-1767
  1. Abstract:

    We hypothesize that innate immune signals from infectious organisms and/or injured tissues may activate peripheral neuronal pain signals. In this study, we demonstrated that TLRs 3, 7, and 9 are expressed by human dorsal root ganglion neurons (DRGNs) and in cultures of primary mouse DRGNs. Stimulation of murine DRGNs with TLR ligands induced expression and production of proinflammatory chemokines and cytokines CCL5 (RANTES), CXCL10 (IP-10), IL-1 alpha, IL-1 beta, and PGE(2), which have previously been shown to augment pain. Further, TLR ligands upregulated the expression of a nociceptive receptor, transient receptor potential vanilloid type 1 (TRPV1), and enhanced calcium flux by TRPV1-expressing DRGNs. Using a tumor-induced temperature sensitivity model, we showed that in vivo administration of a TLR9 antagonist, known as a suppressive oligodeoxynucleotide, blocked tumor-induced temperature sensitivity. Taken together, these data indicate that stimulation of peripheral neurons by TLR ligands can induce nerve pain. The Journal of Immunology, 2011, 186: 6417-6426.

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External Sources

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  2. DOI: 10.4049/jimmunol.1001241
  3. View record in Web of Science®
  4. WOS: 000290755700041

Library Notes

  1. Fiscal Year: FY2010-2011
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