title: Deficient intracellular killing of bacteria by murine alveolar macrophages.
abstract: Microbiologic methods were used to assess the in vitro phagocytosis and intracellular killing of various species of bacteria by freshly isolated murine peritoneal and alveolar macrophages. Peritoneal macrophages showed effective phagocytosis of opsonized Streptococcus pneumoniae, Streptococcus pyogenes, Pseudomonas aeruginosa, Staphylococcus epidermidis, and Listeria monocytogenes, and moderate ingestion of Staphylococcus aureus and Escherichia coli. Alveolar macrophages were poor in phagocytosing opsonized S. pyogenes, S. aureus, and E. coli; ingestion of S. pneumoniae, P. aeruginosa, and S. epidermidis was moderate. Peritoneal macrophages killed 40 to 80% of these bacteria intracellularly, but alveolar macrophages showed almost no intracellular killing of bacteria. To find out whether there is a correlation between the poor bactericidal activity of alveolar macrophages and the oxygen-dependent microbicidal mechanisms of these cells, we determined the uptake of oxygen and the release of superoxide anion and hydrogen peroxide by macrophages at rest and after stimulation with phorbol myristate acetate (PMA) or opsonized S. aureus. Upon exposure to these stimuli, peritoneal macrophages, but not alveolar macrophages, showed an increased uptake of oxygen and release of superoxide anion and hydrogen peroxide. Because alveolar macrophages contain surface active material (SAM), we investigated the phagocytosis and intracellular killing of bacteria and the release of hydrogen peroxide by peritoneal macrophages pretreated with SAM. The results showed reduced phagocytosis and impaired intracellular killing of S. epidermidis by these macrophages. The release of hydrogen peroxide by SAM-pretreated peritoneal macrophages upon stimulation with PMA or opsonized S. aureus was equal to that of the control peritoneal macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
authors.forename: P H
authors.initials: PH
authors.lastname: Nibbering
authors.forename: M T
authors.initials: MT
authors.lastname: van den Barselaar
authors.forename: J S
authors.initials: JS
authors.lastname: van de Gevel
authors.forename: P C
authors.initials: PC
authors.lastname: Leijh
authors.forename: R
authors.initials: R
authors.lastname: van Furth
mesh_terms: D000818:Animals; D001419:Bacteria / Q000276:immunology*; D006861:Hydrogen Peroxide / Q000378:metabolism; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology; D008297:Male; D051379:Mice; D010101:Oxygen Consumption; D010529:Peritoneal Cavity / Q000382:microbiology; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000276:immunology* / Q000382:microbiology; D011951:Receptors, Complement / Q000276:immunology; D017463:Receptors, Complement 3b; D011961:Receptors, Fc / Q000276:immunology
chemical_list: D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D011961:Receptors, Fc; D006861:Hydrogen Peroxide