tosho
16.09.07, 17:11
Znalazlem jakies ciekawe informacje na Lymenecie na temat leku propranolol:
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Published online before print April 16, 2007, 10.1073/pnas.0607263104
PNAS | April 24, 2007 | vol. 104 | no. 17 | 7247-7252
BIOLOGICAL SCIENCES / MICROBIOLOGY
Borrelia burgdorferi intercepts host hormonal signals to regulate expression
of outer surface protein A
Mark R. Scheckelhoff*, Sam R. Telford, Mary Wesley*, and Linden T. Hu*,
*Division of Geographic Medicine and Infectious Diseases, Tupper Research
Institute, Tufts–New England Medical Center, Boston, MA 02111; and Division of
Infectious Diseases, Cummings School of Veterinary Medicine, Tufts University,
Grafton, MA 01536
Edited by John J. Mekalanos, Harvard Medical School, Boston, MA, and approved
March 18, 2007 (received for review August 23, 2006)
The Borrelia burgdorferi infectious cycle requires that the organism adapt to
vast differences in environmental conditions found in its tick and mammalian
hosts.
Previous studies have shown that B. burgdorferi accomplishes this accomodation
in part by regulating expression of its surface proteins. Outer surface
protein A (OspA) is a borrelial protein important in colonization of the tick
midgut.
OspA is up-regulated when the organism is in its tick host and down-regulated
when it is in a mammalian host.
However, little is known about how it is up-regulated again in a mammalian
host in preparation for entry into a feeding tick.
Here, we report that the host neuroendocrine stress hormones, epinephrine and
norepinephrine, are specifically bound by B. burgdorferi and result in
increased expression of OspA.
This recognition is specific and blocked by competitive inhibitors of human
adrenergic receptors.
To determine whether recognition of catecholamines, which are likely to be
present at the site of a tick bite, may play a role in preparing the organism
for reentry into a tick from a mammalian host, we administered a -adrenergic
blocker, propranolol, to infected mice.
Propranolol significantly reduced uptake of B. burgdorferi by feeding ticks
and decreased expression of OspA in B. burgdorferi recovered from ticks that
fed on propranolol-treated mice.
Our studies suggest that B. burgdorferi may co-opt host neuroendocrine signals
to inform the organism of local changes that predict the presence of its next
host and allow it to prepare for transition to a new environment.
MALARIA AN OLD DRUG WITH A HIDDEN TALENT
Researchers at Northwestern University say that they have discovered a way to
get around resistance to standard malaria treatment, one that won't reguire
the development of an expensive new drug. Propranolol, a 40 year old medicine
for high blood pressure, stope the parasites that cause malaria from hijacking
the red blood cells they use to prolifereate.
A researcher team led by Dr. K decided that instead of attacking the parasite
directly, they would block its entry into blood cells. Working with mice, they
discovered that the beta-blocker propranolol caused red blood cells to reject
the parasite. Left exposed, the parasites in propranolol-treated animals could
be killed with on-tenth the amount of antimalarial medicine normally required.
