Elastase-induced pulmonary emphysema: insights from experimental models

Anais da Academia Brasileira de Ciências

Mariana A. Antunes¹  Patricia R.m. Rocco¹ 

[1] ,Universidade Federal do Rio de Janeiro Instituto de Biofísica Carlos Chagas Filho Centro de Ciências da Saúde Laboratório de Investigação PulmonarRio de Janeiro RJ ,Brasil

关键词: chronic obstructive pulonary disease;    elastase;    ephysea;    experiental odel;    soke;    doença pulmonar obstrutiva crônica;    elastase;    enfisema;    modelo experimental;    fumaça;   

DOI  :  10.1590/S0001-37652011005000039

来源: SciELO

【 摘 要 】

Several distinct stimuli can be used to reproduce histological and functional features of human emphysema, a leading cause of disability and death. Since cigarette smoke is the main cause of emphysema in humans, experimental researches have attempted to reproduce this situation. However, this is an expensive and cumbersome method of emphysema induction, and simpler, more efficacious alternatives have been sought. Among these approaches, elastolytic enzymes have been widely used to reproduce some characteristics of human cigarette smoke-induced disease, such as: augmentation of airspaces, inflammatory cell influx into the lungs, and systemic inflammation. Nevertheless, the use of elastase-induced emphysema models is still controversial, since the disease pathways involved in elastase induction may differ from those occurring in smoke-induced emphysema. This indicates that the choice of an emphysema model may impact the results of new therapies or drugs being tested. The aim of this review is to compare the mechanisms of disease induction in smoke and elastase emphysema models, to describe the differences among various elastase models, and to establish the advantages and disadvantages of elastase-induced emphysema models. More studies are required to shed light on the mechanisms of elastase-induced emphysema.

【 授权许可】

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