The disease can be triggered in susceptible people by a variety of environmental contaminants - such as cigarette smoke, allergens and airborne pollution.
Dr. Marsha Wills-Karp and her colleagues have identified the pro-inflammatory protein, interleukin-17 (IL-17A), as the molecular tipping point that upsets a delicate balance between underlying mild disease and more severe asthma, reports Nature.
Airway exposure to environmental allergens causes dysfunctional regulation of a gene called complement factor 3 (C3). This leads to overzealous production of IL-17A by airway cells and sets off what the scientists describe as an "amplification loop," when IL-17A in turn induces more C3 production at the airway surface.
The amplification loop perpetuates increasing inflammatory responses as well as airway hyper-responsiveness and airflow obstruction.
As the team continues their research, they will study the relationship between C3 and IL-17A in severe asthmatics, and explore the effectiveness of targeting either the C3 or IL-17A pathways for the treatment of severe asthma.
The study is published in the latest Nature Immunolog.