Abstract
Previously, we found that inflammatory mediators modulated the number and binding affinity of glucocorticoid receptors (GR) in human bronchial epithelial cell lines. In this study we investigated whether smoking and chronic obstructive pulmonary disease (COPD), both characterized by airway inflammation with increased levels of inflammatory mediators, affect GR characteristics in cultured human bronchial epithelial cells (HBEC). A statistically significant difference was found between the dissociation constant (Kd) values in HBEC from smoking (Kd = 0.98+/-0.08 nM; n = 6) and nonsmoking controls (Kd = 0.76+/-0.10 nM, P = 0.03; n = 5), but no significant difference was found between the mean number of binding sites. Our results are the first indication that cultured HBEC from smokers possess GR with a lower binding affinity. This may result from the inflammation found in the airways from smokers. Furthermore, these results provide further evidence that the bronchial epithelium may be an actual target for inhaled glucocorticoid therapy.
Highlights
The bronchial epithelium has long be en re garde d as a pas sive barrier to protect the underlying tissue .1 bronchial epithelial cells are know n to play an ac tive role in airw ay inflammation
The pre senc e of GR prote in w as demonstrate d using Weste rn blot analysis and 3H-dex ame thasone binding studies
A significant decre as e w as found in the binding affinity of GR in human bronchial epithelial ce lls (HBEC) from smoking c ontrols compare d w ith nonsmoking controls, but no signific ant differe nc e w as found be tw e en the mean numbe r of spec ific glucocortic oid binding site s
Summary
The bronchial epithelium has long be en re garde d as a pas sive barrier to protect the underlying tissue .1 bronchial epithelial cells are know n to play an ac tive role in airw ay inflammation. Gluc oc orticoids are w ide ly used in the tre atment of inflammatory pulmonary dise ase s, e.g. bronchial asthma and chronic obstruc tive pulmonary disease (COPD)[6] Rec ent studie s show ed that glucoc ortic oids are able to inhibit the re le as e of some bronchial epithe lial ce ll-derived cytokines.[3,7] These effe cts of gluc ocorticoids combined w ith the above-mentione d role of bronchial epithelial cells in airw ay inflammation, sugge st that glucocorticoid therapy may suppre ss airw ay inflammation, at least partially, by modulating the func tion of bronchial ep ithe lial cells. This hypothesis is supported by the observation that the greater part of inhale d gluc oc ortic oids pre c ipitate
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