Reduced Nasal Brain Derived Neurotrophic Factor in Aspirin Exacerbated Respiratory Disease
Saturday, March 5, 2016
South Exhibit Hall H (Convention Center)
Michele Pham, MD, Rachel Baum, BS, David Broide, MB,ChB, FAAAAI, Andrew White, MD, FAAAAI, Taylor Doherty, MD, FAAAAI

Aspirin-exacerbated respiratory disease (AERD) is a complex syndrome of eosinophilic sinus inflammation and asthma characterized by hypersensitivity reactions to COX-1 inhibition. Neurotrophins may contribute to inflammatory responses as previous studies have revealed an elevation in brain derived neutrotrophic factor (BDNF) levels in allergic airway disease. Further, TSLP and IL-33 have known roles in promoting eosinophilic tissue inflammation.  However, levels of IL-33, TSLP, and BDNF in AERD have not been reported. 


Nasal lavage (17 patients), blood (32 patients), and urine (45 patients) samples were obtained from AERD patients. Samples from normal controls (11 patients) were also obtained. For AERD patients, samples were collected at the initial visit, after aspirin desensitization, and greater than 30 days after aspirin desensitization. ELISAs were performed with urine, serum, and nasal lavage for BDNF, IL33, and TSLP. 


Only BDNF levels in nasal lavage samples were different and showed reduced levels (p=0.0005) in AERD patients compared with normal controls. There were no differences in BDNF, IL33, or TSLP levels pre and post aspirin desensitization. 


Recent data suggests upregulation of BDNF in severe asthma and previous studies have demonstrated elevated BDNF in chronic sinusitis. In AERD, our data demonstrates lower BDNF levels in nasal secretions. There are a variety of factors that may affect BDNF which include concomitant medications and the unique inflammatory nature of AERD. It is also possible that the reduction in BDNF is a result of counter-regulatory factors in the disease process or related to anosmia found in these patients.