title: Borrelia burgdorferi induces inflammatory mediator production by murine microglia.
abstract: Lyme disease has been associated with damaging inflammation within the central nervous system. In the present study, we demonstrate that Borrelia burgdorferi is a significant stimulus for the production of IL-6, TNF-alpha, and PGE(2) by microglia. This effect is associated with induction of NF-kappaB, and increased expression of Toll-like receptor 2 and CD14, receptors known to underlie spirochete activation of other immune cell types. These studies identify microglia as a previously unappreciated source of inflammatory mediator production following challenge with B. burgdorferi. Such production may play an important role during the development of Lyme neuroborreliosis.
authors.affiliation: Department of Biology, 9201 University City Boulevard, University of North Carolina at Charlotte, 28223, Charlotte, NC, USA.
authors.forename: Amy
authors.initials: A
authors.lastname: Rasley
authors.forename: Juan
authors.initials: J
authors.lastname: Anguita
authors.forename: Ian
authors.initials: I
authors.lastname: Marriott
mesh_terms: D000818:Animals; D025065:Borrelia burgdorferi / Q000276:immunology* / Q000472:pathogenicity; D002461:Cell Line, Transformed; D002490:Central Nervous System / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D051546:Cyclooxygenase 2; D015232:Dinoprostone / Q000378:metabolism; D029721:Drosophila Proteins; D005455:Fluorescent Antibody Technique; D005786:Gene Expression Regulation / Q000276:immunology; D018836:Inflammation Mediators / Q000276:immunology*; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D007527:Isoenzymes / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000235:genetics / Q000276:immunology; D020852:Lyme Neuroborreliosis / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology; D051379:Mice; D008809:Mice, Inbred C3H; D017628:Microglia / Q000276:immunology* / Q000382:microbiology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics; D011451:Prostaglandin-Endoperoxide Synthases / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000235:genetics / Q000276:immunology; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation / Q000276:immunology; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D029721:Drosophila Proteins; D018836:Inflammation Mediators; D015850:Interleukin-6; D007527:Isoenzymes; D018950:Lipopolysaccharide Receptors; D008562:Membrane Glycoproteins; D016328:NF-kappa B; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D051195:Toll-Like Receptor 2; D051193:Toll-Like Receptors; D014409:Tumor Necrosis Factor-alpha; D051546:Cyclooxygenase 2; D011451:Prostaglandin-Endoperoxide Synthases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D015232:Dinoprostone