Borrelia burgdorferi induces inflammatory mediator production by murine microglia.
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.
Rasley
Amy
A
Department of Biology, 9201 University City Boulevard, University of North Carolina at Charlotte, 28223, Charlotte, NC, USA.
Anguita
Juan
J
Marriott
Ian
I
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
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