Chronic obstructive pulmonary disease c 3

Chronic obstructive pulmonary disease c 3

7 Pages · 2002 · 122 KB ·

review of the animal models used to study emphysema is presented. pounds into lungs of animals has been used to emphysema. J Clin Invest 2000;106:1081–93. 50 D'Armiento three different C57 BL/6J mutants. Lab Invest 

Chronic obstructive pulmonary disease c 3 free download

REVIEW SERIES Chronic obstructive pulmonary diseasec3: Experimental animal models of pulmonary emphysema R Mahadeva , S D Shapiro \ Thorax 2002;57:908±914 The use of genetically manipulated mice together with traditional animal studies are steadily increasing our knowledge of the factors important in determining alveolar formation and destruction in emphysema A review of the animal models used to study emphysema is presented \ C hronic obstructive pulmonary disease (COPD) is one of the commonest reasons for ill health worldwide, with 16 million individuals affected in the USA alone It is ranked as the fourth and ®fth highest cause of death in the USA and UK, respectively, with a mortality rate at least 14 times that of asthma 12The single most important factor in the development of emphysema is cigarette smoke Inhalation of cigarette smoke causes a chronic pulmonary in¯ammatory in®ltrate of macrophages, neu trophils and CD8+ cells that persists long after smoking cessation In susceptible individuals this ultimately leads to irreversible destruction and dilatation of the terminal airspaces of the lung, chronic disability due to respiratory failure, and premature death Animal studies have been critical in shaping contemporary views regarding the pathogenesis of emphysema Almost 40 years ago Gross reported that intratracheal instillation of the plant proteinase papain into rats resulted in emphysema This, combined with the clinical observation by Eriksson that de®ciency of the antiproteinase a 1antitrypsin was associated with early onset panlobular emphysema in humans, 34 fuelled the concept that an imbalance within the lung favouring proteinases over their inhibitors resulted in emphysema As more sophisticated animal models have evolved, they have continued to develop fresh insights into lung biology and enabled the testing of novel treatments for emphysema While the initial association of emphysema with a 1antitrypsin de®ciency sug gested that neutrophil derived proteinases were critical to the development of emphysema, recent studiesÐlargely in animal modelsÐhave broad ened the scope of cells and proteinases that may cause emphysema Particular attention has been given to macrophage derived matrix metallopro teinases (MMPs) 5Furthermore, stemming from the study of alveogenesis in experimental ani mals, retinoic acid treatment has been shown to regenerate alveoli in rats both during develop ment and following experimental emphysema 6It is now clear that complex interacting pathways are involved in the initiation, progression, and the failure of correct repair in emphysema While hypotheses and mechanisms of emphy sema can be addressed in the test tube and cell culture, ultimately these ideas need to be tested in mammals to elucidate the complex pathophysiol ogy of COPD Rodents, dogs, guinea pigs, mon keys, and sheep have all been used to study emphysema With the advent of genetic engineer ing in mice, this species offers the greatest ability to dissect pathogenetic pathways in mammals In addition, more is known about its genome than any other animal and cDNA and antibody probes are abundant They also offer the practical bene®ts of short breeding times, large litters, and relatively cheap housing The main issue con founding the use of mice and other animals as a template for human disease is that we do not know how accurately they re¯ect human biology and pathology Mouse and man clearly share many basic physiological processes, but the details of how gas exchange is achieved will determine how closely ®ndings in mice can be applied to man Each animal model should be viewed as one component of the process for studying human disease and not viewed in isola tion or extrapolated directly to humans Emphysema can be modelled in many ways Exogenous administration of proteinases, chemi cals, particulates, and exposure to cigarette smoke result in features characteristic of human COPD Genetic manipulation itself can result in airspace enlargement during development and through out life These different approaches each have their own merits and limitations and require individualised interpretation The methods also often complement each other so their usefulness can be enhanced by using a combination of approaches to study the disease The ®eld has also not infrequently been stimulated by the inadvert ent generation of emphysema in animals where experiments were initially undertaken for an other reason EMPHYSEMA PRODUCED BY CHALLENGE WITH EXOGENOUS AGENTS Intrapulmonary challenge with injurious pro teins, chemicals, particulates, and other com pounds into lungs of animals has been used to cause emphysema directly Compounds have

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