Similarities of host defense mechanisms against pulmonary infectious diseases in animals and man.

Abstract

Evidence linking exposure to air pollutants with increased susceptibility to infectious diseases in humans comes from epidemiological, clinical, and experimental laboratory studies. The data suggest that the most common, and perhaps the most sensitive, index of the pulmonary effect of air pollutant exposure is on post upper respiratory infection, prolonged cough, phlegm, and purulent sputum. Experimental models of these relationships for extrapolation to humans should be able to measure such minor changes in symptomatology and physiology rather than require major lethal events. The bacterial aerosol model for quantifying nonspecific defense mechanisms of the bronchopulmonary tree utilizing nonpathogenic organisms fulfills this criterion. The function of the six major components of pulmonary antimicrobial defense mechanisms--including aerodynamic filtration, secretory respiratory tract fluid, fluid transport at the alveolar and bronchial levels, the phagocytic function of alveolar macrophages, the augmenting mechanisms of blood-derived inflammatory cells, and the secretory and cellular-specific immune mechanisms and their mediator products--can all be quantified by this experimental animal model system. The defensive functions are remarkably similar across animal species, and available human data suggest that findings obtained using the model may be extrapolated to humans.