Aqui vão mais alguns detalhes sobre febre.
From:
Cláudio
Lima
Pesquisadores descobrem mecanismo
que gera a febre
Uma
equipe de cientistas norte-americanos descobriu onde o processo da febre
inicia no cérebro e como esse mecanismo age para nos proteger contra
infecções e doenças. De acordo com os pesquisadores
do Centro Médico Beth Israel Deaconess, nos Estados Unidos,
durante os períodos de inflamação, o corpo produz
hormônios chamados citoquinas, que agem nos vasos sangüíneos
do cérebro para a produção de outro hormônio,
o PGE2. É esse que vai causar a febre, além de perda de apetite,
fatiga e dores no corpo, ao interagir com um receptor de neurônios
chamado E3 na região do cérebro conhecida como hipotálamo.
Todas essas reações, segundo eles, são respostas adaptativas
do organismo para o combate da infecção, por isso, muitas
doenças apresentam os mesmos sintomas.
----
Date: 8/6/2007
Contact: Bonnie Prescott
Phone:
617-667-7306
Email: bprescot@bidmc.harvard.edu
BOSTON – With the finding that fever is produced
by the action of a hormone on a specific site in the brain, scientists
have answered a key question as to how this adaptive function helps to
protect the body during bacterial infection and other types of illness.
Reported by researchers at Beth Israel Deaconess Medical
Center (BIDMC), the study results appear today in Nature Neuroscience’s
Advance Online Publication. “This study shows
how the brain produces fever responses during infections,” explains senior
author Clifford Saper, MD, PhD, Chairman of the Department of Neurology
at BIDMC and James Jackson Putnam Professor of Neurology and Neuroscience
at Harvard Medical School. “Our laboratory identified the key site in the
brain at which a hormone called prostaglandin E2 (PGE2) acts on a target,
called the EP3 receptor, on neurons to cause the fever response.” During
periods of inflammation, such as when the body is fighting an infection
or illness, the body produces hormones known as cytokines. The cytokines,
in turn, act on blood vessels in the brain to produce PGE2. “PGE2
then enters the brain’s hypothalamus, causing fever, loss of appetite,
fatigue and general feelings of sickness and achiness,” says Saper, explaining
that these common symptoms of illness function as an adaptive response
to enable the body to better fight infection. “When
body temperature is elevated by a few degrees, white blood cells can fight
infections more effectively. Also, individuals tend to become achy and
lethargic. Consequently,” he adds, “they tend to take it easy, thereby
conserving their energy so that they can better fight the infection. That
is why so many different types of illness result in more or less the same
sickness behaviors.” To this point, the specific
neurons on which PGE2 was acting to produce fever were unknown. Saper and
his colleagues created a knockout mouse in which the gene for the EP3 receptor
– which registers the presence of PGE2 – could be removed in one part of
the brain at a time. “This was the first time
that anyone has been able to remove the receptor at a single spot in the
brain,” says Saper. “As a result, we are able to definitively say that
this particular site in the brain – only a little bigger than the head
of a pin – is where prostaglandins work to cause the fever response. “We
think that the other aspects of sickness behavior, such as the achiness
caused by increased sensitivity to pain, also come from specific sites
in the brain,” he adds. “We plan to use this same approach to dissect the
brain’s response to inflammation, and find out why people feel the way
they do when they are ill.” This study was funded
by grants from the U.S. Public Health Service. In
addition to Saper, coauthors include BIDMC investigators Michael Lazarus,
PhD (lead author), Kyoko Yoshida, PhD, Takatoshi Mochizuki, PhD, Bradford
Lowell, MD, PhD, and Roberto Coppari, PhD; and Caroline Bass, PhD, of Wake
Forest University, North Carolina. Beth Israel
Deaconess Medical Center is a patient care, teaching and research affiliate
of Harvard Medical School and ranks third in National Institutes of Health
funding among independent hospitals nationwide. BIDMC is clinically affiliated
with the Joslin Diabetes Center and is a research partner of the Dana-Farber/Harvard
Cancer Center. BIDMC is the official hospital of the Boston Red Sox. For
more information, visit www.bidmc.harvard.edu.
Um grande
abraço, Cláudio
Lima - Terapeuta Naturalistahttp://www.reformadesaude.orgMSN:
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