miércoles, 24 de mayo de 2017

Virus linked to food sensitivity | National Institutes of Health (NIH)

Virus linked to food sensitivity | National Institutes of Health (NIH)

National Institutes of Health (NIH) - Turning Discovery into Health

Virus linked to food sensitivity

At a Glance

  • Researchers found that a seemingly innocuous virus can provoke immune responses to a dietary protein in mice.
  • Patients with celiac disease showed high levels of antibodies to the virus.
  • The results suggest that viruses may play a role in initiating immune responses against gluten.
The reovirus core structure. Core structure of a reovirus. Once thought to be harmless, reovirus infections may prompt sensitivity to dietary proteins. Karin M. Reinisch, Max L. Nibert and Stephen C. Harrison, Nature.
Celiac disease is a digestive disorder that’s triggered by eating foods containing gluten—a protein common in foods such as bread, pasta, cookies, and cakes. When a person with celiac disease eats or drinks anything with gluten, the body’s immune system attacks the inside of the small intestine. The damage from this attack keeps the body from absorbing needed nutrients. If left untreated, celiac disease can lead to malnutrition, anemia, weakened bones, and other problems.
Researchers don’t know exactly what triggers celiac disease. Certain genes and other factors, such as things in the environment, can lead to celiac disease. Viral infections have been suggested as a possible trigger.
A team led by Dr. Bana Jabri at the University of Chicago and Dr. Terence S. Dermody at the University of Pittsburgh School of Medicine investigated whether a common but harmless type of virus that people are frequently exposed to, called reoviruses, can prompt sensitivity to dietary proteins. The study was supported by NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and National Institute of Allergy and Infectious Diseases (NIAID), among others. Results were published in Science on April 7, 2017.
The team studied two different strains of reoviruses (T1L, which can infect the intestine, and T3D-RV, which was engineered to infect the intestine) in mice. Both strains triggered an immune response that protected the mice against the infection. However, animals infected with TL1 also showed altered immune responses in the gut. Both type 1 interferon (IFN) signaling and interferon regulatory factor 1 (IRF1) expression increased.
IRF1 regulates gene transcription and plays a key role in oral tolerance, or the suppression of immune responses to an orally delivered substance, like food. After being infected with T1L, susceptible mice lost their oral tolerance to a dietary protein. A follow-up gene expression analysis showed this was triggered by specific changes in immune signaling molecules. These changes both block the mechanism that maintains tolerance to dietary proteins and promote the immune reaction against them.
The team next investigated whether patients with celiac disease had been exposed to reoviruses. Patients with celiac disease had higher levels of reovirus antibodies than controls. Patients on a gluten-free diet also had higher levels of reovirus antibodies and IRF1 levels in their small intestines, suggesting reovirus infection may lead to long-lasting gene expression changes.
“This study clearly shows that a virus that is not clinically symptomatic can still do bad things to the immune system and set the stage for an autoimmune disorder, and for celiac disease in particular,” Jabri says. “However, the specific virus and its genes, the interaction between the microbe and the host, and the health status of the host are all going to matter as well.”
More work will be needed to better understand how reovirus and possibly other viruses might provoke food intolerance. The results may lead to new prevention and treatment strategies.
―Tianna Hicklin, Ph.D.

Related Links

References: Reovirus infection triggers inflammatory responses to dietary antigens and development of celiac disease. Bouziat R, Hinterleitner R, Brown JJ, Stencel-Baerenwald JE, et al., Science. 2017 Apr 7;356(6333):44-50. doi: 10.1126/science.aah5298. PMID: 28386004.
Funding: NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institute of Allergy and Infectious Diseases (NIAID), and National Cancer Institute (NCI); Bettencourt Schueller Foundation; Dutch Sophia Research Foundation; and Austrian Science Fund.

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