zonulin and autoimmune disorders

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Zonulin Could Be Linked To Many Autoimmune Ills

Researchers at the University of land School of Medicine have found that

the human protein zonulin, which regulates the permeability of the

intestine, is at increased levels during the acute phase of celiac disease.

The discovery suggests that increased levels of zonulin are a contributing

factor to the development of celiac disease and other autoimmune disorders

such as insulin dependent diabetes, multiple sclerosis, and rheumatoid

arthritis. The findings are published in the April 29 issue of the journal

Lancet.

" Zonulin works like the traffic conductor or the gatekeeper of our body's

tissues, " says lead author Alessio Fasano, M.D., professor of pediatrics and

physiology at the University of land School of Medicine, and director of

Pediatric Gastroenterology and Nutrition at the University of land

Hospital for Children. " Our largest gateway is the intestine with its

billions of cells. Zonulin opens the spaces between cells allowing some

substances to pass through while keeping harmful bacteria and toxins out, "

explains Dr. Fasano.

Earlier research conducted by Dr. Fasano discovered that zonulin is also

involved in the regulation of the impenetrable barrier between the blood

stream and the brain, known as the blood-brain barrier.

Celiac disease offered Dr. Fasano and his team a unique model for

understanding the dynamic interaction between zonulin and the immune system.

Celiac disease is a genetic disorder that affects one out of every 300

people in Europe, but its prevalence in the United States is not fully

known.

People who suffer from the disorder are unable to eat foods that contain the

protein gluten, which is found in wheat and other grains. The gluten sets

off a reaction that can cause diarrhea, abdominal pain, malabsorption of

nutrients, and other gastrointestinal problems. Celiac disease can be easily

treated by avoiding foods with gluten.

With celiac disease, the body reacts to gluten by creating antibodies that

attack the intestine and cause severe damage over time. Unlike other

autoimmune disorders, scientists also know that celiac disease is triggered

by a specific antigen, which is the protein gluten.

Celiac disease is also known to cause increased permeability of the

intestine. In addition, many people who suffer from celiac disease also

suffer from other autoimmune disorders.

The research team examined the intestinal tissue of seven people with celiac

disease, and six patients without the disease. Patients with active celiac

disease showed higher levels of zonulin and anti-zonulin antibodies compared

to non-celiac patients and patients in remission, who were eating a

gluten-free diet.

" With celiac disease, we could never understand how a big protein like

gluten was getting through to the immune system. Now we have the answer, "

explains Dr. Fasano. " People with celiac have an increased level of zonulin,

which opens the junctions between the cells. In essence, the gateways are

stuck open, allowing gluten and other allergens to pass. Once these

allergens get into the immune system, they are attacked by the antibodies, "

adds Dr. Fasano.

" I believe that zonulin plays a critical role in the modulation of our

immune system. For some reason, the zonulin levels go out of whack, and that

leads to autoimmune disease, " explains Fasano.

Dr. Fasano adds that more research is needed. He is currently conducting

experiments with diabetic rats. Preliminary results from his experiments

show that insulin dependent diabetes occurs in lab rats about three to four

weeks after increased intestinal permeability. The researchers believe the

increased intestinal permeability is associated with increased levels of

zonulin.

" We are at the threshold of exciting discoveries in this field, " says Dr.

Fasano. " We now have a new way of looking at our cells. Our cells are not

stacked together like bricks. They are a dynamic field, which is constantly

in flux. "

[Contact: Tim Parsons, Ellen Beth Levitt]

01-May-2000

Source: http://unisci.com/stories/20002/0501004.htm

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