Abstract

Brain-derived neurotrophic factor (BDNF) and its tropomyosin-related kinase B (TrkB) receptor might contribute to normal lung functioning and immune responses; however, their role in asthma remains unclear. Plasma BDNF concentrations, as well as BDNF and NTRK2 (TrkB gene) polymorphisms, were investigated in 120 asthma patients and 120 healthy individuals using enzyme-linked immunosorbent assay and polymerase chain reaction, respectively. The genotype and allele frequencies of BDNF Val66Met (rs6265) and NTRK2 rs1439050 polymorphisms did not differ between healthy individuals and asthma patients, nor between patients grouped according to severity or different asthma phenotypes. Although plasma BDNF concentrations were higher among healthy subjects carrying the BDNF Val66Met GG genotype compared to the A allele carriers, such differences were not detected in asthma patients, suggesting the influences of other factors. Plasma BDNF concentration was not affected by NTRK2 rs1439050 polymorphism. Asthma patients had higher plasma BDNF concentrations than control subjects; however, no differences were found between patients subdivided according to asthma severity, or Type-2, allergic, and eosinophilic asthma. Higher plasma BDNF levels were observed in asthma patients with aspirin sensitivity and aspirin-exacerbated respiratory disease. These results suggest that plasma BDNF may serve as a potential peripheral biomarker for asthma, particularly asthma with aspirin sensitivity.

Highlights

  • Asthma is a chronic inflammatory disease of the airways characterized by the hallmark features of airway hyperresponsiveness, enhanced bronchial smooth muscle cell contractility, and mucus overproduction [1]

  • Our findings indicate that asthma patients have higher plasma brain-derived neurotrophic factor (BDNF) levels than healthy subjects

  • The genotype and allele frequencies of BDNF Val66Met and NTRK2 rs1439050 polymorphisms did not differ between healthy individuals and asthma patients, nor between patients grouped according to severity or different asthma phenotypes

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Summary

Introduction

Asthma is a chronic inflammatory disease of the airways characterized by the hallmark features of airway hyperresponsiveness, enhanced bronchial smooth muscle cell contractility, and mucus overproduction [1]. It is very common, affecting approximately 235 million children and adults worldwide [2], and causes tremendous morbidity, mortality, and global socioeconomic burden in both Europe [3] and the United States [4]. The remarkable heterogeneity of asthma is underpinned by its wide range of clinical presentations, disease severity, and responses to therapy, as well as the involvement of different pathophysiological mechanisms and biological pathways [5]. BDNF actions are mediated via binding to its high affinity receptor located within the cell membrane, tropomyosin-related kinase B (TrkB) [8,9,10], causing the activation of the downstream MAPK, PI3K, and PLCγ signaling pathways [11,12,13]

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