Biomedical subjects
C E Brightling
Publications and source records attributed to C E Brightling.
Eosinophilic bronchitis is an important cause of chronic cough.
Eosinophilic bronchitis presents with chronic cough and sputum eosinophilia, but without the abnormalities of airway function seen in asthma. It is important to know how commonly eosinophilic bronchitis causes cough, since in contrast to cough in patients without sputum eosinophilia, the cough responds to inhaled corticosteroids. We investigated patients referred over a 2-yr period with chronic cough, using a well-established protocol with the addition of induced sputum in selected cases. Eosinophilic bronchitis was diagnosed if patients had no symptoms suggesting variable airflow obstruction, and had normal spirometric values, normal peak expiratory flow variability, no airway hyperresponsiveness (provocative concentration of methacholine producing a 20% decrease in FEV(1) ([PC(20)] > 8 mg/ml), and sputum eosinophilia (> 3%). Ninety-one patients with chronic cough were identified among 856 referrals. The primary diagnosis was eosinophilic bronchitis in 12 patients, rhinitis in 20, asthma in 16, post-viral-infection status in 12, and gastroesophageal reflux in seven. In a further 18 patients a diagnosis was established. The cause of chronic cough remained unexplained in six patients. In all 12 patients with eosinophilic bronchitis, the cough improved after treatment with inhaled budesonide 400 micrograms twice daily, and in eight of these patients who had a follow-up sputum analysis, the eosinophil count decreased significantly, from 16.8% to 1.6%. We conclude that eosinophilic bronchitis is a common cause of chronic cough, and that sputum induction is important in the investigation of cough.
Development of irreversible airflow obstruction in a patient with eosinophilic bronchitis without asthma.
Eosinophilic bronchitis is a recently described condition presenting with chronic cough and sputum eosinophilia without the abnormalities of airway function seen in asthma. The patient, a 48-yr-old male who had never smoked, presented with an isolated chronic cough. He had normal spirometric values, peak flow variability and airway responsiveness, but an induced sputum eosinophil count of 33% (normal <1%). Although his cough improved with inhaled corticosteroids the sputum eosinophilia persisted. Over 2 yrs he developed airflow obstruction, which did not improve following nebulized bronchodilators and a 2-week course of prednisolone 30 mg once daily sufficient to return the sputum eosinophilia to normal (0.5%). It is suggested that the progressive irreversible airflow obstruction was due to persistent structural change to the airway secondary to eosinophilic airway inflammation, and it is further speculated that eosinophilic bronchitis may be a prelude to chronic obstructive pulmonary disease in some patients.
Inhaled corticosteroids in COPD.
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Isoprenaline inhibits thromboxane B2 release from U937 cells.
The U937 monocytic cell line and its differentiated macrophage-like form have been well characterized, illustrating many similarities with their analogous in vivo cells. We examined the release of thromboxane B2 (TXB2) from undifferentiated and differentiated cells after stimulation with opsonized zymosan and investigated whether the release of this mediator could be modified by isoprenaline. After stimulation, the U937 cells released TXB2 in a dose-dependent manner, with the release greater from the differentiated cells. The TXB2 released was inhibited by flurbiprofen (> 10(-8) M; P < .01) and isoprenaline (> 10(-6) M; P < .01), and the inhibition was reversed by propranolol (10(-6) M; P < .02). Thus, it is clear that undifferentiated and differentiated U937 cells release TXB2, which can be inhibited by beta 2-adrenoceptor stimulation. These findings illustrate an important functional difference between the in vivo macrophages and differentiated U937 cells because beta 2-adrenoceptor stimulation does not inhibit mediator release from macrophages.