title: Interferons direct an effective innate response to Legionella pneumophila infection.
abstract: Legionella pneumophila remains an important opportunistic pathogen of human macrophages. Its more limited ability to replicate in murine macrophages has been attributed to redundant innate sensor systems that detect and effectively respond to this infection. The current studies evaluate the role of one of these innate response systems, the type I interferon (IFN-I) autocrine loop. The ability of L. pneumophila to induce IFN-I expression was found to be dependent on IRF-3, but not NF-kappaB. Secreted IFN-Is then in turn suppress the intracellular replication of L. pneumophila. Surprisingly, this suppression is mediated by a pathway that is independent of Stat1, Stat2, Stat3, but correlates with the polarization of macrophages toward the M1 or classically activated phenotype.
authors.affiliation: Department of Biological Sciences, Columbia University, New York, New York 10032, USA.
authors.forename: Courtney R
authors.initials: CR
authors.lastname: Plumlee
authors.forename: Carolyn
authors.initials: C
authors.lastname: Lee
authors.forename: Amer A
authors.initials: AA
authors.lastname: Beg
authors.forename: Thomas
authors.initials: T
authors.lastname: Decker
authors.forename: Howard A
authors.initials: HA
authors.lastname: Shuman
authors.forename: Christian
authors.initials: C
authors.lastname: Schindler
mesh_terms: D000818:Animals; D019898:Autocrine Communication / Q000276:immunology; D002478:Cells, Cultured; D007113:Immunity, Innate; D007370:Interferon Type I / Q000276:immunology*; D007372:Interferons / Q000276:immunology*; D016952:Legionella pneumophila / Q000502:physiology; D007877:Legionnaires' Disease / Q000276:immunology*; D008262:Macrophage Activation; D008264:Macrophages / Q000166:cytology / Q000276:immunology; D051379:Mice; D016328:NF-kappa B; D050791:STAT Transcription Factors
chemical_list: D007370:Interferon Type I; D016328:NF-kappa B; D050791:STAT Transcription Factors; D007372:Interferons