title: Pulmonary macrophage function during experimental cytomegalovirus interstitial pneumonia.
abstract: Since cytomegalovirus (CMV) infections may alter host defense against a variety of pathogens, phagocytosis, oxygen uptake, and H2O2 release by pulmonary macrophages obtained from guinea pigs with acute CMV interstitial pneumonia were evaluated. Experimental animals were inoculated subcutaneously on day zero with 10(7.5) 50% tissue culture infective doses of virulent guinea pig CMV. Control animals received an uninfected salivary gland suspension. The animals were sacrificed on day 7; the tissues were cocultivated for virus isolation, and the lungs were lavaged to obtain pulmonary macrophages. CMV was isolated from buffy coat cells (96%), bone marrow cells (71%), whole lungs (77%), pulmonary macrophages (60%), and pulmonary granulocytes (49%). There was no significant difference between groups at sacrifice in the total number of macrophages obtained by pulmonary lavage or in the phagocytic activity of the macrophages in vitro. However, in CMV-infected animals, the maximum rates of O2 consumption in response to the soluble stimulus, phorbol myristate acetate, and the particulate stimulus, Staphylococcus aureus, were 47 and 55%, respectively, of the rates in uninfected controls. Total macrophage O2 consumption in CMV-infected animals was 32 and 37%, respectively, of control values in response to the same stimuli. In CMV-infected animals, the maximum rates of H2O2 release were 22% of those in simultaneous controls for both stimuli, and total H2O2 release was 30 and 25%, respectively, of that in controls in response to these stimuli. Such alterations in macrophage oxidative function may contribute to superinfection during CMV pneumonia.
authors.forename: S A
authors.initials: SA
authors.lastname: Miller
authors.forename: F J
authors.initials: FJ
authors.lastname: Bia
authors.forename: D L
authors.initials: DL
authors.lastname: Coleman
authors.forename: H L
authors.initials: HL
authors.lastname: Lucia
authors.forename: K R
authors.initials: KR
authors.lastname: Young
authors.forename: R K
authors.initials: RK
authors.lastname: Root
mesh_terms: D000208:Acute Disease; D000818:Animals; D003587:Cytomegalovirus / Q000472:pathogenicity; D003586:Cytomegalovirus Infections / Q000276:immunology*; D006168:Guinea Pigs; D006861:Hydrogen Peroxide / Q000378:metabolism; D008168:Lung / Q000382:microbiology; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology; D010101:Oxygen Consumption; D010587:Phagocytosis; D011658:Pulmonary Fibrosis / Q000276:immunology* / Q000382:microbiology
chemical_list: D006861:Hydrogen Peroxide