Pulmonary Clearance of Infectious Agents

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Abstract
The lung is equipped with defensive mechanisms for inactivating or removing inhaled inert or infectious particles. The health of the lung may be determined by the functional state of these defenses. A major area of defense is against inhaled infectious agents which are unique as particles because of their capacity to increase in mass and number. Whereas transport mechanisms in the alveoli and bronchi may have long-range import for the disposition of the remains of infectious particles, the necessity for rapid inactivation of the viability of the organism places a premium on the performance of microbicidal mechanisms. In the noninflamed lung, the primary microbicidal mechanism appears to be the alveolar macrophage. Unsuccessful performance by this system leads to inflammation. The functional state of the alveolar macrophage system is influenced by genetic endowment, prior immunologic experience, metabolic state of the host, presence of diseases in other systems, concurrent pulmonary disease, and simultaneous activity of a large number of exogenous agents that alter macrophage activity. Factors which alter macrophage activity may affect its behavior in a highly specific manner, as in specific immunity; or nonspe-cifically, as in toxic poisoning, where defense against a broad spectrum of infectious and nonliving materials may be altered. The alveolar macrophage is a logical final common pathway for the expression of genetic, metabolic, biochemical, immunological, and toxicologlcal physiology in its interaction with inert, allergenie, or infectious agents of the external environment. This pathway is central to the defense of the lung against infectious agents, and may be central in the genesis of pulmonary pathology.