Conclusion

Although it is somewhat difficult to differentiate age-associated changes in the structure and function of the aging human lung from environmentally induced lung disorders and genetic susceptibility to lung disease, changes in the lung matrix that alter airway and parenchymal structure, which some investigators have termed ''senile emphysema'' or ductasia, appear to be a generalized phenomenon that occurs in the absence of environmental risk factors. These changes lead to a decline in elastic recoil and altered ventilation to perfusion relationships that affect pulmonary function testing values and gas exchange. The precise cause of these changes is not clear, but similar changes have been shown in the lungs of aged mice or dogs. The investigation of cellular compartment turnover, matrix alterations, and the role of cytokines such as VEGF, which can have a profound effect on the microvasculature, in these animal models may provide additional insights into the age-associated processes that alter the structure and function of the aging human lung. Models that seem particularly attractive for such investigations are aged C57/Bl mice, the SAM mouse, and Beagle dogs. Animal models may also help to identify age-associated factors that put the elderly at an increased risk for acute events such as pneumonia. Relatively little is known about innate immune mechanisms in the aged human lung, for one, and such models could facilitate the study of age-associated changes in innate immunity that may increase the risk of lower respiratory tract infection in the elderly and provide strategies to prevent pneumonia.

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