Short report: Association of macrophage inflammatory response and cell death after in vitro Borrelia burgdorferi infection with arthritis resistance. Am J Trop Med Hyg 2006 Nov;75(5):964-7
Date
11/25/2006Pubmed ID
17123997DOI
10.4269/ajtmh.2006.75.964Scopus ID
2-s2.0-34247192311 (requires institutional sign-in at Scopus site) 14 CitationsAbstract
Susceptibility to Borrelia burgdorferi infection and subsequent arthritis is genetically determined in mice and determined by innate immunity. Accordingly, macrophage responses to B. burgdorferi challenge may differ between mouse strains. Bone marrow-derived macrophages were infected ex vivo with clonal B. burgdorferi strain N40. Interleukin-12 and tumor necrosis factor-alpha (TNF-alpha) production were higher in macrophages from resistant C57Bl/6 mice than in macrophages from susceptible C3H/HeJ mice. However, TNF-alpha production was observed in lower concentrations in C3H/HeJ (toll-like receptor-4(-/-)) macrophages than in C3H/FeJ (TLR4(+/+)) macrophages, suggesting that TLR4 might contribute to the response to B. burgdorferi. A higher cytokine response to B. burgdorferi was associated with cell death in macrophages from resistant C57Bl/6 mice. Understanding variability in the response of macrophages to B. burgdorferi may contribute to understanding Lyme arthritis.
Author List
Glickstein LJ, Coburn JLAuthor
Jenifer Coburn PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsArthritis, Infectious
Borrelia burgdorferi
Cells, Cultured
Joints
Lyme Disease
Macrophage Activation
Macrophages
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Knockout