Chili peppers and inflammation: researchers
unravel mechanism of pain sensitivity
BOSTON - September 25, 2002 - Scientists at Massachusetts
General Hospital (MGH) have discovered a common component to the
burning sensation produced by chili peppers and the pain associated
with arthritis. The finding, published in the September 26 issue
of Neuron, could help scientists devise new strategies to
block the pain hypersensitivity associated with inflammation.
"The receptor activated by chili peppers in the mouth and
other tissues also increases in the terminals of sensory neurons
in the skin after inflammation, and this contributes to pain hypersensitivity,"
says Clifford Woolf, MD, PhD, director of the Neural Plasticity
Research Group in the Department of Anesthesia and Critical Care
at MGH. A receptor is a protein that transports a chemical signal
into a cell.
Woolf and lead author Ru-Rong Ji, PhD, also of the MGH Neural Plasticity
Research Group, found that the increased production of the receptor
following inflammation is mediated by a signal molecule called p38,
located within sensory neurons. The chili pepper receptor, which
is technically called TRPV1, responds to capsaicin, the chemical
that is responsible for the "hot" in peppers. It also
responds to actual heat and to low pH, a condition that occurs with
"With these findings, we're starting to understand why patients
with arthritis or other inflammatory conditions are likely to have
increased pain and sensitivity to heat," says Woolf, who also
is Richard J. Kitz Professor of Anaesthesia Research at Harvard
Medical School. He and his research team were surprised to find
that the activation of p38 can cause a twenty-fold increase in the
amount of TRPV1 protein in the skin but not in the activity of the
gene coding for TRPV1.
"This means that the chili pepper receptor is not being regulated
by the gene being switched on but by more protein being produced,
an unexpected form of regulation," says Ji. He also notes that
their findings will open up new options for pain management. "We
could use an inhibitor to p38 to block the increase in TRPV1, therefore
blocking pain in patients who suffer from many diseases and conditions
that involve inflammation."
Following inflammation, the activation of p38 is very precise.
The scientists found that it is caused by a specific growth factor
signal acting on a particular subset of pain sensory neurons. There
are a variety of pain sensations that create different changes within
neurons, and all of the signals that are generated have not yet
been identified. Each new discovery, like the current finding by
the MGH researchers, sheds light on these complex pathways and brings
new treatment strategies closer.
The other members of the MGH research team are Tarek Samad, PhD,
San-Xue Jin, PhD, and Raymond Schmoll, MS, all of the MGH Neural
Plasticity Research Group. The study was supported by grants from
the National Institutes of Health.
Massachusetts General Hospital, established in 1811, is the original
and largest teaching hospital of Harvard Medical School. The MGH
conducts the largest hospital-based research program in the United
States, with an annual research budget of more than $300 million
and major research centers in AIDS, cardiovascular research, cancer,
cutaneous biology, transplantation biology and photomedicine.
In 1994, the MGH joined with Brigham and Women's Hospital to form
Partners HealthCare System, an integrated health care delivery system
comprising the two academic medical centers, specialty and community
hospitals, a network of physician groups and nonacute and home health
Media Contact: Susan
McGreevey , MGH Public Affairs
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