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Molecular Referees Offer Insight on Aspirin-Induced Disease
BWH's Joshua Boyce (at right) works with researcher Tao Liu, PhD, (left) to study the characteristics of a common lung condition.
Aspirin is usually taken to relieve aches and pains, but sometimes it's the culprit behind certain diseases. One such disease, known as aspirin-exacerbated respiratory disease, is a common respiratory condition that occurs in people with asthma who have sensitivity to aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs).
Aspirin-exacerbated respiratory disease affects 5 to 10 percent of adults with asthma, around 30 percent of people with severe asthma, and approximately 40 percent of people with asthma plus nasal polyps. New research provides insight into how the disease manifests, as well as novel treatment options.
Too Much, Too Little
One of the characteristics of aspirin-exacerbated respiratory disease is the overproduction of cysteinyl leukotrienes-one of many chemical ‘referees' that regulate the body's inflammatory response. Overproduction of these regulators leads to disease-related respiratory symptoms, such as constriction of the airway passages in the lungs.
Also, the respiratory system's negative reaction to aspirin prevents another type of inflammatory response regulator, known as prostaglandin E2, from being produced and working properly.
"Decreased production of prostaglandin E2 with inflammation in pre-clinical models is remarkably similar to the effects of aspirin-exacerbated respiratory disease in humans," said Joshua Boyce, MD, director of the Inflammation and Allergic Diseases Section in the Department of Rheumatology, Immunology and Allergy, and senior study author. "This study also strongly suggests that the body's inability to make normal amounts of prostaglandin E2 likely causes the disease."
Targeted Treatment
Knowing that abnormal prostaglandins play a role in causing aspirin-exacerbated respiratory disease, researchers found that introducing stable prostaglandins blocked the respiratory system's negative reactions to aspirin by about 90 percent.
Moreover, disease symptoms such as airway resistance and lung inflammation were reduced by drugs that targeted certain cells and cell receptors involved in the overproduction of the chemical referees.
"These experiments reveal that platelet [a type of blood cell] dysfunction may underlie the characteristic overproduction of cysteinyl leukotrienes," said Boyce. "Drugs which interfere with platelets or with prostaglandin receptors hold promise in treating aspirin-exacerbated respiratory disease."