We examined the lipid content of bronchoalveolar (BA) washes from both mice and rats infected with Mycoplasma pulmonis, an etiological agent of murine pneumonia. During a 30-day period after intranasal inoculation, the total lipid content from infected and control rats (in milligrams per animal) remained relatively equal and unchanged. The saturated, unsaturated, and total lecithin contents in infected rats (in milligrams per animal) all increased. The maximum lecithin values were detected at 7 to 10 days after infection; later, the levels fell to control values. There was essentially no change in any lecithin value from uninfected animals. Although in BA washes from infected animals the mass of disaturated lecithins increased, the percentage of this fraction in the total lecithin pool decreased. The fatty acids of the lecithins from BA washes of infected mice had significantly less palmitic and significantly more oleic and linoleic acids than the lecithins isolated from the BA washes of control animals. Both the relative decrease in the mass of disaturated lecithins in the BA washes and the increase in the percentage of esterified unsaturated fatty acids in the lecithins may be directly related to the reduced lung function reported to occur during the course of murine M. pulmonis pneumonia.Excised lungs from rodents infected with a mycoplasma or influenza virus are more difficult to distend, i.e. have lower pulmonary compliance, than those from animals free of respiratory disease (22,53). There are two major determinants of lung compliance: surface tension at the air-tissue interface and elasticity of the lung tissue. In the case of these infections, the lower compliance was due primarily to increased surface tension rather than to changes in the elasticity of lung tissue. Loosli et al. (25) also have shown a decrease in the pulmonary surface properties of mice infected with influenza virus A.Pulmonary surfactant, a lipoprotein material which coats the alveolar walls, is responsible for decreasing surface tension at the air-tissue interface in lungs (31). By decreasing alveolar surface tension, surfactant reduces the work required to inflate the lungs. Surfactant also promotes alveolar stability at low lung volumes and minimizes pulmonary transcapillary pressure gradients (30). An increase in surface tension is reflected by a decrease in the compliance of the lungs.Klaus et al. (21) established that the active material in pulmonary surfactant is a phospholipid. The major active component has been identified as a disaturated lecithin, dipalmitoyl phosphatidylcholine (4,19,29,64). It is not clear whether other components of pulmonary surfactant contribute to the modification of surface forces occurring in situ or of those observed in experiments using alveolar washes (18,20,26,45). Several investigators have demonstrated a relationship between changes in lung compliance and either respiratory infection or altered lung surfactant, or both. Hakuno (13) found low surface activity and lowered levels of saturated fatty...