Thursday, September 19, 2013
In a surprise finding likely to alter
how neurologists, immunologists and microbiologists view infection-associated
pain, a group at Boston Children's Hospital has shown that bacteria can directly trigger action
potentials in pain fibers, leading to the release of neuropeptides that
suppress the inflammatory response.1 The findings point to a role
for sensory neurons as immune modulators and could provide new bacterial
targets for pain.
The therapeutic targets identified by
the paper are the bacterial proteins FMIFL and aHL or their points of
entry, FPR1 and ADAM10. However, based on ongoing research, Woolf believes that
these may represent only two of several bacterial protein mediators of pain.
Thus, he thinks hitting these targets may have only a limited analgesic effect.
Fishburn, C.S. SciBX 6(36); doi:10.1038/scibx.2013.982
Published online Sept. 19, 2013
1. Chiu, I.M. et al.
Nature; published online Aug. 21, 2013; doi:10.1038/nature12479
Contact: Clifford J. Woolf, Boston Children's Hospital and Harvard
Medical School, Boston, Mass.
2. Nicotra, L. et al.
Exp. Neurol. 234, 316-329 (2012)
3. Rivière, S. et al.
Nature 459, 574-577 (2009)
AND INSTITUTIONS MENTIONED
Boston Children's Hospital, Boston, Mass.
Harvard Medical School, Boston, Mass.
Stanford University, Palo Alto, Calif.
University of California, San Diego, La Jolla, Calif.
University of Pittsburgh School of Medicine, Pittsburgh, Pa.