title: Alteration of pulmonary macrophage function by respiratory syncytial virus infection in vitro.
abstract: Alveolar macrophages (AL) are the first line of defense against inhaled pathogens and are exposed to virus during the course of a respiratory syncytial virus (RSV) infection. Interference of virus with alveolar macrophage functions may contribute to the risk of acquiring secondary bacterial infections during or after respiratory tract infections with RSV or other viral agents. We studied whether murine AL get infected with RSV and whether they support viral replication in vitro. In addition, the effects of RSV on microbicidal and on immunoregulatory functions were examined. Only a subpopulation of AL expressed viral F proteins after exposure of these cells to RSV. Infected AL released only small amounts of infectious virus into the supernatant. The extent of virus replication in AL seemed to be dependent in part on the amount of IFN induced by the virus, as has been demonstrated by infection of lung tissue macrophages and AL in vitro. In general, RSV infection of pulmonary macrophages appeared to be abortive. Nevertheless, release of reactive oxygen intermediates, phagocytosis, and killing of protozoa were reduced in RSV-infected AL in comparison to noninfected AL. In contrast, RSV stimulated secretion of TNF-alpha, IL-1, and IL-6 in an infectious-dose dependent manner. Along with the increased cytokine release, accessory functions of AL were increased after RSV exposure. Thus, exposure of AL to RSV appeared to stimulate their immunoregulatory functions, whereas the microbicidal activity of these cells seemed to be severely diminished.
authors.affiliation: Fraunhofer Institute for Toxicology and Molecular Research, Department of Immunology, Hannover, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Franke-Ullmann
authors.forename: C
authors.initials: C
authors.lastname: Pförtner
authors.forename: P
authors.initials: P
authors.lastname: Walter
authors.forename: C
authors.initials: C
authors.lastname: Steinmüller
authors.forename: M L
authors.initials: ML
authors.lastname: Lohmann-Matthes
authors.forename: L
authors.initials: L
authors.lastname: Kobzik
authors.forename: J
authors.initials: J
authors.lastname: Freihorst
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D005260:Female; D007375:Interleukin-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D007893:Leishmania donovani; D008070:Lipopolysaccharides / Q000494:pharmacology; D008262:Macrophage Activation; D016676:Macrophages, Alveolar / Q000502:physiology / Q000821:virology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010587:Phagocytosis; D016897:Respiratory Burst; D012136:Respiratory Syncytial Viruses / Q000502:physiology*; D012441:Saccharomyces cerevisiae; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D014779:Virus Replication
chemical_list: D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha