Transgenic and gene-targeted mice as models for chronic obstructive pulmonary disease

Factors resulting in airspace enlargement in mice. Mice may obtain enlarged airspaces due to abnormal development or destruction of mature alveoli. Failed septation during alveogenesis occurring in transgenic mice might have biological importance if the overexpressed protein has the capacity to be overexpressed in human lung development. Abnormal alveogenesis in knockout mice suggests that the product is made and if, for some reason, lost, this could result in disease. Neither mechanism is directly relevant to pulmonary emphysema, which is defined by destruction of airspaces that were previously normal. This phenotype may be observed in mice via one of the following: by inducing a transgene during adulthood, spontaneous occurrence over time in gene-targeted mice, and by administering a relevant injurious agent (e.g. cigarette smoke) to gene-targeted mice. The mice can then be compared with wildtype mice to determine a role in chronic obstructive pulmonary disease.