Increased circulating β₂-adrenergic receptor autoantibodies are associated with smoking-related emphysema.

ABSTRACT: Smoking is a dominant risk factor for chronic obstructive pulmonary disease (COPD) and emphysema, but not every smoker develops emphysema. Immune responses in smokers vary. Some autoantibodies have been shown to contribute to the development of emphysema in smokers. β₂-adrenergic receptors (β₂-ARs) are important targets in COPD therapy. β₂-adrenergic receptor autoantibodies (β₂-AAbs), which may directly affect β₂-ARs, were shown to be increased in rats with passive-smoking-induced emphysema in our current preliminary studies. Using cigarette-smoke exposure (CS-exposure) and active-immune (via injections of β₂-AR second extracellular loop peptides) rat models, we found that CS-exposed rats showed higher serum β₂-AA

SUBMITTER: Hu JY 

PROVIDER: S-EPMC5338268 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature