PGE2 decreases muscle cell proliferation in patients with non-asthmatic eosinophilic bronchitis

Non-asthmatic eosinophilic bronchitis (NAEB) is characterized by chronic cough and sputum eosinophilia without bronchial hyperresponsiveness. The aim of the present study is to determine whether increased levels of PGE2 from NAEB sputum supernatants play a protective role in airway inflammation and muscular hyperplasia. Twenty-one patients with NAEB, 15 asthmatic patients, and 12 healthy subjects were studied. An up-regulated PGE2 enzymatic pathway was observed in bronchial biopsies from patients with NAEB as compared with samples from asthmatic patients. Also, EP2 and EP4 receptor expression was increased in these samples. BSMC proliferation was inhibited to a greater extent in NAEB sputum supernatants than in those taken from asthmatic subjects and healthy controls. This inhibition was mostly due to PGE2 levels, a fact which was confirmed by employing synthetic EP2 and EP4 agonist and antagonist receptors.These findings suggest that PGE2 inhibits BSMC proliferation entailing a reduction of smooth muscle hyperplasia and thus protecting against the onset of airflow obstruction.

► Asthma in contrast to NAEB is characterized by airway hyperresponsiveness.
► PGE2 level in induced sputum is strikingly increased in subjects with NAEB.
► PGE2 is able to inhibit BSMC proliferation through the EP2 and EP4 receptors.
► PGE2 attenuates muscular hyperplasia.
► PGE2 can exert protective effects in lungs by binding to EP2 and EP4 receptors.