Inflammation In Rheumatoid Arthritis
- From: mark_denton2006@xxxxxxxxx
- Date: 24 Feb 2006 16:06:55 -0800
Unexpected Discovery Made By Scientists Exploring Inflammation In
Rheumatoid Arthritis
Arthritis News
Article Date: 20 Feb 2006
BOSTON -- What makes joints in people with rheumatoid arthritis, and
related conditions like Lyme disease or lupus, so susceptible to attack
by the body's immune system, leading to painful flare-ups and
deterioration? The answer may surprise you.
The answer did surprise investigators at Joslin Diabetes Center and
Massachusetts General Hospital (MGH) in Boston, who gained a novel
insight into this question in a recent collaborative study. Their
report appeared in the January 29 online issue of Nature Immunology,
and is scheduled to appear in the February print edition.
Working with an animal model of rheumatoid arthritis, the researchers
discovered that histamine, a small molecule usually associated with
asthma and allergy, is produced as part of the inflammatory process
during the development of arthritis. Histamine made the blood vessels
surrounding the joints especially vulnerable to leakage, and thereby
rendered the joints more susceptible to inflammatory attack. The
researchers believe that this is true not only in rheumatoid arthritis,
but perhaps also in other autoimmune conditions with which arthritis is
associated, such as lupus, and in some infectious diseases, like Lyme
disease.
"For patients with rheumatoid arthritis, these new findings raise the
possibility that medications designed to prevent the blood vessels from
becoming leaky might one day be used to delay the onset of arthritis or
to prevent flare-ups of disease," said Christophe Benoist, M.D., Ph.D.,
who led the study together with Diane Mathis, Ph.D., and Ralph
Weissleder, M.D., Ph.D. Drs. Mathis and Benoist head Joslin?s Section
on Immunology and Immunogenetics, hold the William T. Young Chair in
Diabetes Research at Joslin, and are Professors of Medicine at Harvard
Medical School. Dr. Weissleder heads the Center for Molecular Imaging
Research at MGH and is a Professor of Radiology at Harvard Medical
School.
While the Joslin lab focuses its work on type 1 diabetes, arthritis has
several related mechanisms. Like type 1 diabetes, rheumatoid arthritis
is an autoimmune disease, in which the body's immune system attacks
itself as though fighting off an enemy invader.
The Arthritis Foundation reports the number of Americans with arthritis
or chronic joint symptoms has risen from 35 million to 66 million
(nearly 1 in 3 adults) in 2005. Rheumatoid arthritis (RA) is a chronic
autoimmune disease characterized by inflammation of the lining, or
synovium, of the joints. It is one of the most severe forms of
arthritis and can lead to long-term joint damage, resulting in chronic
pain, loss of function and disability. RA affects 1 percent of the U.S.
population or 2.1 million Americans, mostly women.
In their study, the researchers developed a new microscopic imaging
method to visualize changes in blood vessel permeability in
anesthetized mice. Within minutes following the delivery of
arthritis-causing antibodies to the mice, the blood vessels around the
joints became temporarily leaky, making it easier for the antibodies to
enter the joint spaces. There, the antibodies set off a cascade of
inflammatory cells and molecules, eventually resulting in arthritis.
"The big surprise was that the other blood vessels throughout the body
did not become leaky, suggesting that there is something special about
the vessels in the joints," says Bryce Binstadt, M.D., Ph.D., of Joslin
and Children's Hospital Boston, lead author on the study.
In trying to identify the special feature, the investigators made the
even more unexpected discovery that histamine was responsible for the
joint blood vessel leakiness -- in fact, the researchers could mimic
the effect of the antibodies on blood vessel leakiness by just
injecting histamine.
Other researchers participating in the study included Pratik R. Patel,
Herlen Alencar, M.D., and Umar Mahmood, M.D., Ph.D., of the Center for
Molecular Imaging Research, Massachusetts General Hospital; Peter A.
Nigrovic, M.D., of Children's Hospital and Brigham and Women?s
Hospital, Boston; and David M. Lee, M.D., Ph.D., of Brigham and Women's
Hospital.
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