2011•The Tohoku Journal of Experimental MedicineOpen access

Tryptase Enzyme Activity Is Correlated with Severity of Chronic Obstructive Pulmonary Disease

Xiaojun Zhang, Honggao Zheng, Wenjing Ma, Fang Wang, Xiaoning Zeng, Changting Liu, Shaoheng He

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Abstract

Tryptic enzymes, including tryptase, a signature enzyme in mast cells, are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic inflammatory airway disease. However, the relationship between tryptase enzyme activity and COPD remains to be investigated. We therefore measured the enzyme activity and immunoreactivity of tryptase in the sputum and plasma of COPD patients in the present study. The results showed that tryptase enzyme activity in the sputum of severe COPD patients (FEV(1)s being recorded at ≤ 30% prediction values) was 3.4 times greater than that in patients with mild COPD (FEV(1)s being recorded at ≥ 80% of predicted values), whereas tryptic activity was 2.0 times higher in the severe COPD patients than in mild COPD patients. Moreover, tryptase enzyme activity, but not tryptic enzyme activity, was significantly elevated in the plasma of severe COPD patients compared with that of mild COPD patients. The level of immunoreactive tryptase was 1.9 times higher in the sputum of the severe COPD patients at admission than that at remission stage. We also employed a rat model of cigarette smoke-induced COPD. After 36 weeks of daily challenges with cigarette smoke, a well-established risk factor of COPD, tryptic and tryptase activities in the bronchoalveolar lavage fluid were elevated 1.5 and 2.6 times, respectively. These results indicate that smoking induces tryptase enzyme activity in the airway. In conclusion, tryptase enzyme activity is markedly increased in sputum and plasma of severe COPD patients. Enhanced tryptase enzyme activity may contribute to the pathogenesis of COPD.

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Tryptic enzymes, including tryptase, a signature enzyme in mast cells, are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic inflammatory airway disease. However, the relationship between tryptase enzyme activity and COPD remains to be investigated. We therefore measured the enzyme activity and immunoreactivity of tryptase in the sputum and plasma of COPD patients in the present study. The results showed that tryptase enzyme activity in the sputum of severe COPD patients (FEV(1)s being recorded at ≤ 30% prediction values) was 3.4 times greater than that in patients with mild COPD (FEV(1)s being recorded at ≥ 80% of predicted values), whereas tryptic activity was 2.0 times higher in the severe COPD patients than in mild COPD patients. Moreover, tryptase enzyme activity, but not tryptic enzyme activity, was significantly elevated in the plasma of severe COPD patients compared with that of mild COPD patients. The level of immunoreactive tryptase was 1.9 times higher in the sputum of the severe COPD patients at admission than that at remission stage. We also employed a rat model of cigarette smoke-induced COPD. After 36 weeks of daily challenges with cigarette smoke, a well-established risk factor of COPD, tryptic and tryptase activities in the bronchoalveolar lavage fluid were elevated 1.5 and 2.6 times, respectively. These results indicate that smoking induces tryptase enzyme activity in the airway. In conclusion, tryptase enzyme activity is markedly increased in sputum and plasma of severe COPD patients. Enhanced tryptase enzyme activity may contribute to the pathogenesis of COPD.

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Available abstract

Tryptic enzymes, including tryptase, a signature enzyme in mast cells, are involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic inflammatory airway disease. However, the relationship between tryptase enzyme activity and COPD remains to be investigated. We therefore measured the enzyme activity and immunoreactivity of tryptase in the sputum and plasma of COPD patients in the present study. The results showed that tryptase enzyme activity in the sputum of severe COPD patients (FEV(1)s being recorded at ≤ 30% prediction values) was 3.4 times greater than that in patients with mild COPD (FEV(1)s being recorded at ≥ 80% of predicted values), whereas tryptic activity was 2.0 times higher in the severe COPD patients than in mild COPD patients. Moreover, tryptase enzyme activity, but not tryptic enzyme activity, was significantly elevated in the plasma of severe COPD patients compared with that of mild COPD patients. The level of immunoreactive tryptase was 1.9 times higher in the sputum of the severe COPD patients at admission than that at remission stage. We also employed a rat model of cigarette smoke-induced COPD. After 36 weeks of daily challenges with cigarette smoke, a well-established risk factor of COPD, tryptic and tryptase activities in the bronchoalveolar lavage fluid were elevated 1.5 and 2.6 times, respectively. These results indicate that smoking induces tryptase enzyme activity in the airway. In conclusion, tryptase enzyme activity is markedly increased in sputum and plasma of severe COPD patients. Enhanced tryptase enzyme activity may contribute to the pathogenesis of COPD.

Key concepts: Tryptase, COPD, Medicine, Bronchoalveolar lavage, Sputum, Pathogenesis, Internal medicine, Gastroenterology

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