Science and Technology
31.08.2010

Identified genetic basis for determining the severity of allergic asthma

Research may help in the search for future therapeutic strategies to combat a growing problem of health

Scientists at Cincinnati Children's Hospital Medical Center, USA, have identified a new genetic basis for determining the severity of allergic asthma in experimental models of disease. The study may help in the search for future therapeutic strategies to combat an increasing health problem that currently lacks effective treatments.

The prevalence of asthma has increased in recent years, according to the study's senior investigator, Marsha Wills-Karp. The disease can be triggered in susceptible people by a variety of environmental contaminants like cigarette smoke, allergens and air pollution.

The team of Wills-Karp found a molecular tipping point that disturbs the delicate balance between the base of mild and more severe asthma. They identified the pro-inflammatory proteins, interleukin-17 (IL-17A) as the main culprit behind severe asthma symptoms in mouse models.

"This study suggests that at some point it may be possible to treat or prevent severe forms of asthma, inhibiting pathways that lead to the production of IL-17A," said Wills-Karp.

The disease process seems to begin when the airway exposure to environmental allergens cause dysfunction in the regulation of a gene called factor com3 (C3), which runs through a part of the immune system called complement cascade activation. This leads to excess production of IL-17A cells in the airways and causes what scientists describe as a "cycle of amplification, when IL-17A in turn induces the production of more C3 on the surface of the airways.

The amplification cycle continues to increase inflammatory response involving T cells irregular, other proteins of interleukin (IL-13 and IL-23) as well as the response in excess of the airways and obstruction to airflow.

Previous studies demonstrated the presence of IL-17A protein in human asthma, but no apparent function. Previous research involving mouse models of disease suggest possible roles for IL-17A in asthma, and this study expands on those findings.

Source: Isaude.net