Faculty Collaboration Database

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

11/25/2006

Pubmed ID

17123997

DOI

10.4269/ajtmh.2006.75.964

Scopus ID

2-s2.0-34247192311 (requires institutional sign-in at Scopus site)   14 Citations

Abstract

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 JL

Author

Jenifer Coburn PhD Professor in the Medicine department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Arthritis, Infectious
Borrelia burgdorferi
Cells, Cultured
Joints
Lyme Disease
Macrophage Activation
Macrophages
Mice
Mice, Inbred C3H
Mice, Inbred C57BL
Mice, Knockout