In:
Scientific Reports, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2017-03-06)
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. β 2 -adrenergic receptors (β 2 -ARs) are important targets in COPD therapy. β 2 -adrenergic receptor autoantibodies (β 2 -AAbs), which may directly affect β 2 -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 β 2 -AR second extracellular loop peptides) rat models, we found that CS-exposed rats showed higher serum β 2 -AAb levels than control rats before alveolar airspaces became enlarged. Active-immune rats showed increased serum β 2 -AAb levels, and exhibited alveolar airspace destruction. CS-exposed-active-immune treated rats showed more extensive alveolar airspace destruction than rats undergoing CS-exposure alone. In our current clinical studies, we showed that plasma β 2 -AAb levels were positively correlated with the RV/TLC (residual volume/total lung capacity) ratio ( r = 0.455, p 〈 0.001) and RV%pred (residual volume/residual volume predicted percentage, r = 0.454, p 〈 0.001) in 50 smokers; smokers with higher plasma β 2 -AAb levels exhibited worse alveolar airspace destruction. We suggest that increased circulating β 2 -AAbs are associated with smoking-related emphysema.
Type of Medium:
Online Resource
ISSN:
2045-2322
Language:
English
Publisher:
Springer Science and Business Media LLC
Publication Date:
2017
detail.hit.zdb_id:
2615211-3
