Distinctive bronchial inflammation status in athletes: basophils, a new player.

The aim of the study was to establish bronchial inflammation status and to measure eicosanoids in sputum obtained from active elite athletes. A total of 68 subjects were enrolled. Twelve were non-athletes and non-asthmatic (NAtNAs), 21 non-athlete asthmatics (NAtAs), 11 athlete non-asthmatics (AtNAs), and 24 athletes with asthma (AtAs) with positive indirect or direct bronchial challenges. Induced sputum was used to measure cells and eicosanoids. Sputum differential cell counts in all the subject groups revealed eosinophilia with the exception of NAtNAs control subjects. Athletes with and without diagnosed asthma showed a significant increase in bronchial epithelial cells and lymphocytes present in their sputum. Also, flow cytometry revealed that a significantly higher number of basophils were present in sputum from athletes (without and with asthma) when compared with non-athletes (without and with asthma). Asthmatic athletes and non-athletes showed a higher increase in LTC(4) levels and PGE(2) metabolites in sputum when compared with healthy controls. The present study identifies basophils as a new player present in athletes bronchial inflammation defining athlete status and not necessarily associated with exercise-induced bronchoconstriction.

PGE(2) 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 PGE(2) 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 PGE(2) 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 PGE(2) levels, a fact which was confirmed by employing synthetic EP2 and EP4 agonist and antagonist receptors.These findings suggest that PGE(2) inhibits BSMC proliferation entailing a reduction of smooth muscle hyperplasia and thus protecting against the onset of airflow obstruction.