I can see this becoming standard operating procedure simply because
it puts the inflammation response somewhat under the intervenor's
control. This is a far cry from a cold compress.
It will certainly block the development of sepsis as a matter of
course. It may even help in flesh eating disease.
This is a nice piece of innovation. I wonder what else the technique
might be applied to.
Bio-hybrid device
acts as 'thermostat' to control systemic inflammation in sepsis
by Staff Writers
Pittsburgh PA (SPX) May 21, 2012
The Vodovotz group
also is creating computer models of inflammation, which could be used
to engineer the next generation of this device. The portability of
the device could be particularly useful on the battlefield, where
early intervention to control systemic inflammation after injury
might improve the chances of survival.
A small, external
bioreactor holding human cells pumped out an anti-inflammatory
protein to prevent organ damage and other complications in a rat with
acute inflammation caused by bacterial products in a model
of sepsis, according to a report from researchers at the University
of Pittsburgh School of Medicine and the McGowan Institute for
Regenerative Medicine. The findings were published today in the
inaugural issue of Disruptive Science and Technology.
Inflammation is a
necessary biological response that brings cells and proteins to the
site of tissue injury to contend with foreign agents, such as
bacteria and the products they produce, and to begin the healing
process, explained senior author Yoram Vodovotz, Ph.D., professor,
Department of Surgery, and director, Center for Inflammation and
Regenerative Modeling at the McGowan Institute.
But sometimes,
the inflammatory response escalates to create damage
on its own, triggering more inflammation in a self-sustaining and
dangerous cycle.
"In sepsis,
for example, the inflammatory response evolves almost too quickly,
but the available treatment strategies aim to prevent inflammation
entirely," he said. "A better approach would be to turn
down the response when it's too strong, yet still have
appropriate inflammation signaling to promote tissue repair."
During inflammation,
the body makes a protein called tumor necrosis factor-alpha,
or TNF-a. It also makes its counterpart, soluble TNF-a receptor, or
sTNFR, which binds to and reduces the level of TNF-a. In some
situations, such as sepsis, not enough sTNFR is made to limit the
inflammatory response.
Dr. Vodovotz and his
team loaded a small bioreactor with human liver cells
engineered to make sTNFR continuously. Through an intravenous
line, blood from an anesthetized rat experiencing acute but
transient inflammation was pumped through the bioreactor, exposing it
to the engineered cells.
When the bioreactor
was loaded with sTNFR-producing cells, sTNFR levels rose beyond what
the animal could produce on its own, while TNF-a levels dropped, as
did other markers of inflammation. The animal's blood pressure also
improved, and markers of organ damage were reduced.
"This bio-hybrid
device acts as a kind of inflammation thermostat," Dr. Vodovotz
said. "By loading it with cells that produce different amounts
of sTNFR, or other inflammatory blockers, we may soon be able to
tailor our interventions to carefully balance inflammation and immune
responses based on the patient's medical situation."
His team now is
exploring the effectiveness of cells engineered to produce sTNFR
based on the individual production of TNF-a, rather than
continuously, in order to create a disease-specific response for each
patient. Such a personalized medicine therapy platform could be
extended based on emerging knowledge regarding the biology of
inflammation.
The Vodovotz group
also is creating computer models of inflammation, which could be used
to engineer the next generation of this device. The portability of
the device could be particularly useful on the battlefield, where
early intervention to control systemic inflammation after injury
might improve the chances of survival.
Co-authors of the
paper include Rami A. Namas, M.D., Maxim Mikheev, M.D., Ph.D.,
Jinling Yin, M.D., Patrick Over, B.S., Matthew Young, B.S., Gregory
M. Constantine, Ph.D., Ruben Zamora, Ph.D., Jorg Gerlach, M.D.,
Ph.D., all from the University of Pittsburgh and the McGowan
Institute. The project was funded by the U.S. Department of Defense,
National Institutes of Health grant P50-GM-53789, and the
Commonwealth of Pennsylvania.
Related Links
University of Pittsburgh Schools of the Health Sciences
Hospital and Medical
News at InternDaily.com
There is a product called hyperimmune egg that adjusts the immune response. It has been subjected to both double blind and clinical studies.
ReplyDeleteHere is a link:
http://dnusbaum.com/immune26/My_story.html