Chronic pain affects millions of people worldwide. A new study presents a promising therapeutic strategy in which Toll-like receptor (TLR) 5 stimulation enables the analgesic compound, QX-314, to specifically enter and silence large fiber sensory neurons, which convey pain in the setting of injury.
References
Finnerup, N.B., Sindrup, S.H. & Jensen, T.S. Pain 150, 573–581 (2010).
Xu, Z.-Z. et al. Nat. Med. 21, 1326–1331 (2015).
Binshtok, A.M., Bean, B.P. & Woolf, C.J. Nature 449, 607–610 (2007).
Roberson, D.P. et al. Nat. Neurosci. 16, 910–918 (2013).
Melzack, R. & Wall, P.D. Science 150, 971–979 (1965).
Campbell, J.N., Raja, S.N., Meyer, R.A. & Mackinnon, S.E. Pain 32, 89–94 (1988).
Li, L. et al. Cell 147, 1615–1627 (2011).
Park, C.K. et al. Neuron 82, 47–54 (2014).
Liu, T., Gao, Y.J. & Ji, R.R. Neurosci. Bull. 28, 131–144 (2012).
Burdelya, L.G. et al. Science 320, 226–230 (2008).
Howell, B.A., et al. CPT Pharmacometrics Syst. Pharmacol. 3, e98 (2014).
Patapoutian, A., Tate, S. & Woolf, C.J. Nat. Rev. Drug Discov. 8, 55–68 (2009).
Acknowledgements
Funding was provided by US National Institutes of Health NS084191, the Rita Allen Foundation and the American Pain Society to R.P.S.
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Peirs, C., Seal, R. Targeting Toll-like receptors to treat chronic pain. Nat Med 21, 1251–1252 (2015). https://doi.org/10.1038/nm.3986
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DOI: https://doi.org/10.1038/nm.3986
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