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Researchers Explore Mechanisms of Allergic Disease

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New research on allergic disease mechanisms was presented today at the

2005 Annual Meeting of the American Academy of Allergy, Asthma &

Immunology in San .

CD14 A POTENTIAL TARGET FOR PROBIOTICS

Researchers have discovered that the molecule CD14 may be a potential

target for preventative measures against atopic disease. These findings

were presented today at the 2005 Annual Meeting of the American Academy

of Allergy, Asthma & Immunology (AAAAI) in San .

Promising results have recently been reported from studies using

probiotics, microbes that beneficially stimulate the host’s immune

system and intestinal microbes, to reduce the risk of atopic disease in

infancy and childhood. However, the mechanisms by which probiotics

might exert their effect remain unclear.

Samuli Rautava, MD, and colleagues from the University of Turku,

FINLAND, investigated the role of the molecule CD14 in the development

of atopic disease. Eighteen infants received a mixture of probiotics

during the first year of life and 20 received a placebo mixture.

Researchers found that probiotics increased the serum level of soluble

CD14 at one year of age compared to infants who received the placebo.

These results suggest that specific probiotics may enhance healthy

hot-microbe interaction through the molecule CD14 and influence the

development of atopic disease in infancy.

NON-CANONICAL GENE SPLICING ESSENTIAL TO AUTOIMMUNE DISEASES

Researchers believe that non-canonical gene splicing is an essential

feature for most proteins involved in autoimmune diseases. These

findings were presented today at the 2005 AAAAI Annual Meeting in San

.

When genes are encoded into proteins, unwanted internal segments are

removed in a process called splicing. The canonical form of splicing

occurs in more than 99% of regular proteins. However, in proteins that

are targets of autoimmune diseases, canonical splicing is significantly

reduced, and another form of splicing called non-canonical splicing

occurs more frequently.

To determine to what extent non-canonical splicing takes place, Bernard

Ng, MD, and colleagues from Baylor College of Medicine, compared 45

randomly selected proteins associated with autoimmune diseases to 9,554

randomly selected proteins from the human genome.

Researchers discovered that 80% of the autoimmune disease proteins

underwent non-canonical splicing, which was significantly higher than

the less than 1% rate found in the human genome proteins. These

findings demonstrate the potential power of mining the human genome

sequence for understanding the molecular mechanisms by which autoimmune

diseases develop. Defining the molecules targeted by the immune system

in these diseases should also enable the development of novel

therapies.

HIGH DOSE OF AN ALLERGEN PREVENTS ALLERGIC SENSITIZATION

A new therapy called high dose allergen exposure may prevent the

development of allergies, according to new research presented at the

2005 AAAAI Annual Meeting in San .

Marc A. Riedl, MD, and colleagues from the Geffen School of

Medicine at UCLA, using a human nasal allergic sensitization model,

examined the effect of nasal allergen dose on the likelihood of

becoming allergic to that specific allergen. A protein called keyhole

limpet hemocyanin (KLH) was used as the model allergen due to its

safety and rare chance of exposure in everyday life.

Allergic individuals completed a series of nasal sprays with varying

doses of KLH. At the end of the study, nasal washes were examined for

allergic antibodies to KLH. Upon examination, researchers discovered:

* At low dose of KLH – 100% of the patients became allergic

* At medium dose of KLH – 57% became allergic

* At high dose of KLH– only 11% developed an allergy

These results suggest that a high dose of an initial exposure to an

allergen may teach the immune system to “tolerate” the allergen rather

than produce an allergic reaction. Future research will test whether

high dose allergen exposure is a useful therapy to prevent allergies

from ever developing in certain individuals.

TOLL-LIKE RECEPTOR 7 PLAYS A ROLE IN DECREASING ASTHMA

The activation of toll-like receptor 7 plays an important role in the

onset of asthma, according to new research presented today at the 2005

AAAAI Annual Meeting in San .

Toll-like receptors activate multiple steps in the inflammatory

reactions that help eliminate invading pathogens and coordinate

systemic defenses. Serder Sel, MD, from Biomedical Research Center,

Marburg, Germany, and colleagues evaluated the impact of toll-like

receptor 7 (TLR-7) activation on established allergen triggered asthma

in mice.

After inducing allergic asthma in mice, researchers administered

injections of R-848, a synthetic TLR-7 ligand. They found that the

TLR-7 ligand completely reversed allergic asthma in the mice. It

suppressed airway eosinophilia, inflammation of the airway mucosa, IgE

production and normalized airway responsiveness.

These studies were presented at the 2005 Annual Meeting of the American

Academy of Allergy, Asthma and Immunology (AAAAI). The AAAAI is the

largest professional medical specialty organization in the United

States representing allergists, asthma specialists, clinical

immunologists, allied health professionals and others with a special

interest in the research and treatment of allergic disease.

Allergy/immunology specialists are pediatric or internal medicine

physicians who have elected an additional two years of training to

become specialized in the treatment of asthma, allergy and immunologic

disease. Established in 1943, the AAAAI has over 6,000 members in the

United States, Canada and 60 other countries. The AAAAI serves as an

advocate to the public by providing educational information through its

Web site, http://www.aaaai.org, and its Physician Referral and

Information Line, 1 (800) 822-2762.

http://www.newswise.com/articles/view/510310/

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