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Official Journal of the Italian Society of Thoracic Endoscopy
Indexed/Abstracted in: EMBASE, Scopus
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
Wright J. L. , Churg A.
In humans, cigarette smoking induces the clinical and pathological conditions of chronic bronchitis, emphysema, bronchiolitis, and pulmonary hypertension. In order to devise novel, and appropriately specific, therapies, it is important to be able to understand the mechanisms involved in the genesis of such disease states. In the past, there have been relatively few animal models which have been based on tobacco smoke administration, but recently, this has become a renewed area of interest. Exposure of laboratory animals to cigarette smoke produces a form of centrilobular emphysema, and considerable detail is emerging about the proteolytic and nonproteolytic pathways involved in these models. In some species cigarette smoke also produces pulmonary hypertension. Although smoke does induce goblet cell metaplasia in the airways in some animals, no good model of chronic bronchitis exists. Similarly, smoke produces inflammatory influxes into the small airways, but as yet there is no animal model that reproduces the small airway lesions seen in humans. Despite these failures, animal models are beginning to shed light on the complex mechanisms behind smoke-induced disease. Use of genetically modified animals has been extremely helpful in elucidating the various processes which lead to tobacco associated lung disease.