Renkema T E, Postma D S, Noordhoek J A, Sluiter H J, Kauffman H F
Dept of Pulmonology, University Hospital, Groningen, The Netherlands.
Eur Respir J. 1993 Jan;6(1):90-5.
Evidence is accumulating that neutrophil-derived oxidants substantially contribute to the development of emphysema, especially in smoking individuals. It is not clear, however, why not all smokers develop emphysema. We tested the hypothesis that an abnormality in the oxidative metabolism of polymorphonuclear leucocytes (PMNs) might contribute to the development of emphysema. We investigated in vitro O2- production by peripheral PMNs in patients with stable emphysema and in healthy controls. In addition, we investigated whether in vivo prednisolone may modulate in vitro O2- production by PMNs in patients with emphysema during a stable phase of the disease. Spontaneous O2- production by PMNs was not significantly different in patients and controls. After stimulation with submaximal concentrations of calcium ionophore A23187 and phorbol myristate acetate, however, PMNs from patients with stable emphysema produced more O2- than those from healthy controls, especially in smoking subjects. Moreover, in vitro O2- generation by PMNs significantly decreased after in vivo prednisolone treatment in patients with emphysema. We suggest that our findings reflect an abnormality of PMNs, acting as one of the factors that contribute to the development of emphysema. This abnormality may, at least partially, be dampened by in vivo prednisolone treatment. These findings may provide new insights into the pathogenesis and treatment of pulmonary emphysema. Further studies on pulmonary PMNs are necessary to extend our findings.
越来越多的证据表明，中性粒细胞衍生的氧化剂在肺气肿的发展过程中起了很大作用，尤其是在吸烟人群中。然而，目前尚不清楚为什么并非所有吸烟者都会患上肺气肿。我们验证了一个假说，即多形核白细胞（PMN）氧化代谢异常可能与肺气肿的发生有关。我们研究了稳定期肺气肿患者和健康对照者外周血PMN的体外产氧情况。此外，我们还研究了在疾病稳定期，体内给予泼尼松龙是否可以调节肺气肿患者PMN的体外产氧。患者和对照者PMN的自发产氧没有显著差异。然而，用次最大浓度的钙离子载体A23187和佛波醇肉豆蔻酸酯乙酸盐刺激后，稳定期肺气肿患者的PMN比健康对照者产生更多的氧，尤其是在吸烟受试者中。此外，肺气肿患者体内给予泼尼松龙治疗后，PMN的体外产氧量显著降低。我们认为，我们的研究结果反映了PMN的异常，这是导致肺气肿发生的因素之一。这种异常可能至少部分地被体内泼尼松龙治疗所抑制。这些发现可能为肺气肿的发病机制和治疗提供新的见解。有必要对肺PMN进行进一步研究以扩展我们的发现。
