Coughing, wheezing, lungs encased in steel (or so they seem) … asthma makes breathing a challenge for nearly 25 million Americans of all ages. Despite the overwhelming number of people affected, this disease continues to be difficult to understand and to treat.
Asthma is divided into two main categories depending on the age of onset. Childhood-onset asthma develops early, before age 16, but may persist as a life-long condition. This subtype of disease is more common in boys than in girls and is often associated with allergies (in some populations). Adult-onset asthma typically develops in middle age and tends to be more prevalent in women than in men. Unlike its early-onset counterpart, later-onset asthma is not necessarily linked to allergy sensitivity and may be more resistant to treatment.
Asthma shows a strong family component, highlighting a role for genetics in a person’s risk for disease development. But, can we find the risky SNPs? In a recent publication from the New England Journal of Medicine, a group of researchers from a large consortium of asthma studies compared genotypes from more than 25,000 people of European ancestry (roughly 10,000 individuals with diagnosed asthma and more than 15,000 unaffected individuals) to determine potential genes involved in different asthma subtypes.
Although many SNPs identified in this investigation are linked to disease risk at any age, results indicate that one gene region on chromosome 17 is specifically associated with childhood-onset asthma only. Even among the SNPs linked with asthma risk in general, nearly all demonstrated a stronger effect in childhood rather than later-onset disease. Data did not reveal any genetic influence contributing uniquely to asthma severity or development risk from workplace exposure. The authors also investigated whether SNPs associated with asthma risk corresponded to SNPs known to regulate allergy sensitivity since the two conditions are often linked. Results suggest very little overlap between these two sets of SNPs, leading the authors to speculate that allergy sensitivity is an effect of asthma rather than its cause.
Many of the SNPs identified in this paper are located in genes associated with the immune system’s communication network. Just like human armies, the cellular infantry of your immune system sends messages to coordinate its attack on harmful invaders. The genes implicated in this study act to communicate alarm signals from damaged airway tissue to immune cells, triggering the airway inflammatory response often associated with an asthmatic attack. This insight into the genetic culprits underlying the development of asthma may help reveal new targets for therapeutic intervention.