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Expression of protease activated receptor-2 (PAR-2) in central airways of smokers and non-smokers
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  1. D Miotto1,
  2. M D Hollenberg2,
  3. N W Bunnett3,
  4. A Papi1,
  5. F Braccioni1,
  6. P Boschetto4,
  7. F Rea5,
  8. A Zuin5,
  9. P Geppetti6,
  10. M Saetta7,
  11. P Maestrelli8,
  12. L M Fabbri9,
  13. C E Mapp4
  1. 1Institute of Respiratory Diseases, University of Ferrara, Italy
  2. 2Departments of Pharmacology, University of Calgary, Canada
  3. 3Department of Physiology, University of California, San Francisco, USA
  4. 4Departments of Experimental and Clinical Medicine, Section of Occupational Medicine, University of Ferrara, Italy
  5. 5Institute of Thoracic Surgery, University of Padova, Italy
  6. 6Departments of Experimental and Clinical Medicine, Pharmacology Section, University of Ferrara, Italy
  7. 7Institute of Respiratory Diseases, University of Padova, Italy
  8. 8Department of Environmental Medicine and Public Health, Section of Occupational Medicine, University of Padova, Italy
  9. 9Departments of Medicine, Oncology and Radiology, Section of Respiratory Diseases, University of Modena, Italy
  1. Correspondence to:
    Dr C E Mapp, Dipartimento di Medicina Clinica e Sperimentale, Sezione di Igiene e Medicina del Lavoro, Via Fossato di Mortara 64/b; 44100 Ferrara, Italy

Abstract

Background: Protease activated receptor-2 (PAR-2) is a transmembrane G protein coupled receptor preferentially activated by trypsin and tryptase. The protease activated receptors play an important role in most components of injury responses including cell proliferation, migration, matrix remodelling, and inflammation. Cigarette smoking causes an inflammatory process in the central airways, peripheral airways, lung parenchyma, and adventitia of pulmonary arteries.

Methods: To quantify the expression of PAR-2 in the central airways of smokers and non-smokers, surgical specimens obtained from 30 subjects undergoing lung resection for localised pulmonary lesions (24 with a history of cigarette smoking and six non-smoking control subjects) were examined. Central airways were immunostained with an antiserum specific for PAR-2 and PAR-2 expression was quantified using light microscopy and image analysis.

Results: PAR-2 expression was found in bronchial smooth muscle, epithelium, glands, and in the endothelium and smooth muscle of bronchial vessels. PAR-2 expression was similar in the central airways of smokers and non-smokers. When smokers were divided according to the presence of symptoms of chronic bronchitis and chronic airflow limitation, PAR-2 expression was increased in smooth muscle (median 3.8 (interquartile range 2.9–5.8) and 1.4 (1.07–3.4) respectively); glands (33.3 (18.2–43.8) and 16.2 (11.5–22.2), respectively); and bronchial vessels (54.2 (48.7–56.8) and 40.0 (36–40.4), respectively) of smokers with symptoms of chronic bronchitis with normal lung function compared with smokers with chronic airflow limitation (COPD), but the increase was statistically significant (p<0.005) only for bronchial vessels.

Conclusions: PAR-2 is present in bronchial smooth muscle, glands, and bronchial vessels of both smokers and non-smokers. An increased expression of PAR-2 was found in bronchial vessels of patients with bronchitis compared with those with COPD.

  • smoking
  • chronic obstructive lung disease
  • bronchitis
  • G protein coupled receptors

https://doi.org/10.1136/thorax.57.2.146

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