Elastase-induced pulmonary emphysema: insights from experimental models

Abstract

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.

Elimination of p19ARF‐expressing cells protects against pulmonary emphysema in mice

“…The PPE‐induced model is highly reproducible but does not capture all features of human emphysema (Antunes & Rocco, 2011). We also observed that cigarette smoking‐induced pulmonary dysfunction was ameliorated by the elimination of p19 ARF ‐expressing cells (data not shown).…”

Mesenchymal Stromal Cells to Regenerate Emphysema: On the Horizon?

“…The most frequently used model where the therapeutic potential of MSCs was studied was intratracheal instillation of pancreatic elastase into mice to induce lung damage mimicking emphysema [15]. Elastase cleaves elastin fibers, leading to a reduced elastin content, and causes alveolar lesions as seen in emphysema patients [16].…”

Efeito do inibidor de proteinase de origem vegetal CrataBL, sobre a lesão pulmonar induzida pela elastase em camundongos C57/BI6

“…As formas de indução do enfisema são divididas entre os modelos de indução por cigarro e indução por elastase. Existem modelos de enfisema induzidos pela elastase que se diferenciam na dose, na quantidade de aplicações, no tempo do protocolo e na forma de aplicação (Antunes, 2011 …”