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Am. J. Trop. Med. Hyg., 75(5), 2006, pp. 964-967
Copyright © 2006 by The American Society of Tropical Medicine and Hygiene

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SHORT REPORT


ASSOCIATION OF MACROPHAGE INFLAMMATORY RESPONSE AND CELL DEATH AFTER IN VITRO BORRELIA BURGDORFERI INFECTION WITH ARTHRITIS RESISTANCE

LISA J. GLICKSTEIN* AND JENIFER L. COBURN
Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Boston, Massachusetts; Division of Geographic Medicine and Infectious Diseases, Tufts-New England Medical Center, Boston, Massachusetts

 

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.

Received May 3, 2006. Accepted for publication June 23, 2006.

Acknowledgments: We thank Dr. Linden Hu for helpful discussions, and Dr. Georg Weber for many insightful suggestions on the manuscript.

Financial support: Lisa J. Glickstein was supported by a grant from the Harold G. and Leila Y. Mathers Foundation. Jenifer L. Coburn was supported by a biomedical science grant from the Arthritis Foundation, National Institutes of Health grants AI-40938 and AI-051407, and by Public Health Service grant 1 P30DK39428 awarded by the National Institute of Diabetes and Digestive and Kidney Diseases to the Center for Gastroenterology Research on Absorptive and Secretory Processes at Tufts-New England Medical Center.

* Address correspondence to Lisa J. Glickstein, Massachusetts General Hospital, 149 13th Street, Room 8301, Charlestown, MA, 02129. E-mail: lglickstein{at}partners.org

Authors’ addresses: Lisa J. Glickstein, Massachusetts General Hospital, 149 13th Street, Room 8301, Charlestown, MA, 02129, Telephone: 617-726-1529, Fax: 617-726-1544, E-mail: lglickstein{at}partners.org. Jenifer L. Coburn, Tufts-New England Medical Center, 750 Washington Street, NEMC Box 41, Boston, MA, 02111, Telephone: 617-636-5952, Fax: 617-636-3216, E-mail: jcoburn{at}tufts-nemc.org.




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