Research
Boost Immune System
A Little Stress May Go A Long Way Toward Boosting Skin's
Immunity
2-9-2004
COLUMBUS, Ohio – A series of studies in rats and mice
suggests that short bouts of stress increase the skin's
ability to fight infections and heal minor wounds.
The
immune response of animals exposed to acute stress –
about two hours of restraint – was two to four times
higher compared to non-stressed animals. This was true when
the animals' skin was treated with chemical or protein antigens
immediately after a stressful event. An antigen is any substance
that the immune system reacts to by producing cells and
antibodies.
Stress
plus exposure to the antigen triggered an immune response
that remained strong for weeks to several months later,
when the animals were re-exposed to the irritant without
further restraint.
"Acutely
stressed animals had a much more vigorous immune response
when they were first exposed to the antigen," said
Firdaus Dhabhar, an associate professor of oral biology
and molecular virology, immunology and medical genetics
at Ohio State University.
"That
boost to immunity seemed to last, as these animals' immune
systems also showed a powerful response when re-exposed
to the antigen much later."
Control
animals showed a normal immune response to the antigen upon
re-exposure, but nowhere near that of the animals that had
been stressed.
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Dhabhar will give an overview of a decade's worth
of research on the effects of acute stress on skin immunity on February
10 at the annual American Academy of Dermatology meeting in Washington,
D.C.
In several laboratory studies, researchers compared
the immune responses of rats and mice that were restrained for two
hours immediately before exposure to the antigen to control animals
that were not restrained.
"Gentle restraint, or confinement, creates psychological
stress," Dhabhar said. "As a result, heart rate increases,
as do blood pressure and circulating levels of stress hormones. All
are characteristic signs of a normal stress response, and all subside
within a few hours after the stressful situation ends."
The researchers assessed the magnitude of immune responses
by measuring the degree of inflammation at the initial site of antigen
administration. They examined the types of cells and proteins –
indicators of immune system activity – that were present, and
in what amounts.
Animals were exposed to the same antigen, this time
at a different place on the body, a few weeks to several months later.
The researchers again measured immune responses.
"The stressed animals had a much more powerful
immune response to the antigen, compared to the non-stressed animals,"
Dhabhar said. "And the stressed animals' immune systems continued
to stay strong, too, as shown by the later tests."
Short-term stress had boosted the animals' immune
responses two to four times over the response of the non-stressed
mice, an effect the researchers saw when the animals were first exposed
to the antigen. The researchers saw the same results when animals
were again exposed to the antigen a few weeks to several months later.
"The more robust initial immune reaction might
have formed a more efficient, or larger, pool of memory cells that
ultimately gave the stressed animals' immune systems a continued immune
advantage months later," Dhabhar said.
Memory cells "remember" a specific antigen
– a substance that the immune system reacts to by forming cells
and antibodies. Years and even decades later memory cells can launch
an intense attack against the same antigen.
Dhabhar likens the body's immune response to waging
a war: Soldiers, in the form of immune cells and proteins, travel
from the barracks (the spleen) through blood-vessel boulevards to
potential battle stations in the skin. This process speeds up during
brief bouts of stress.
"During both the initial and secondary exposures,
the stressed animals' immune responses occurred at a faster rate and
were significantly elevated for several days compared to control animals,"
Dhabhar said, adding that while this effect may be beneficial for
healing a wound and fighting infections, it could also spell trouble
for people with skin allergies or inflammatory disorders such as eczema,
dermatitis, psoriasis and arthritis.
"In many of these diseases, the immune system
attacks the body and causes inflammation and other serious problems,"
Dhabhar said. "Anything that boosts the immune response can cause
more damage. But learning how the immune system mobilizes these inflammation-causing
cells could possibly help scientists develop therapeutic targets for
such diseases."
Learning how the body mobilizes an immune response
during stress could also give researchers insight into creating more
effective vaccines.
"The whole point of vaccination is to generate
more memory cells," Dhabhar said. "The way the stressed
animals' immune systems responded to the antigen the second time around
suggests that acute stress may help generate more of these memory
cells.
"Most people believe that stress weakens the
immune system and increases susceptibility to infection, yet the benefits
of acute stress make sense from an evolutionary standpoint,"
he said. "Short-term stress activates protective biological mechanisms
that are essential for survival."
Support for this work came from the National Institutes
of Health and The Dana Foundation Clinical Hypotheses Program in Mind
Body Medicine.
This
story has been adapted from a news release issued by Ohio State University,
www.osu.edu.
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