Brain, Vol. 124, No. 8, 1544-1554,
August 2001
© 2001 Oxford University Press
Bacterial peptidoglycan and immune reactivity in the central nervous system in multiple sclerosis
1 Departments of Immunology and 2 Neurology, Erasmus University and University Hospital Rotterdam-Dijkzigt, Rotterdam and 3 Netherlands Brain Bank, Amsterdam, The Netherlands
Correspondence to:
J. D. Laman, Department of Immunology, Erasmus University, Rotterdam, PO Box 1738, 3000 DR Rotterdam, The Netherlands E-mail: laman{at}immu.fgg.eur.nl
Multiple sclerosis is believed to result from a CD4+ T-cell response against myelin antigens. Peptidoglycan, a major component of the Gram-positive bacterial cell wall, is a functional lipopolysaccharide analogue with potent proinflammatory properties and is conceivably a mediator of sterile inflammation. Here we demonstrate that peptidoglycan is present within antigen-presenting cells in the brain of multiple sclerosis patients. These cells have macrophage and dendritic cell characteristics, and are immunocompetent as evidenced by co-expression of inflammatory cytokines and co-stimulatory molecules. In addition, intrathecal plasma cells specific for peptidoglycan are present in multiple sclerosis brain tissue, and antibodies binding peptidoglycan are present in CSF during active disease. Peptidoglycan may thus contribute to T- and B-cell activity during brain inflammation without a requirement for local bacterial replication.
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
J. Lindsey and S. Patel Review: PCR for bacterial 16S ribosomal DNA in multiple sclerosis cerebrospinal fluid Multiple Sclerosis, March 1, 2008; 14(2): 147 - 152. [Abstract] [PDF] |
||||
![]() |
C. Marik, P. A. Felts, J. Bauer, H. Lassmann, and K. J. Smith Lesion genesis in a subset of patients with multiple sclerosis: a role for innate immunity? Brain, November 1, 2007; 130(11): 2800 - 2815. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Herrmann, M. Kellert, A. Spreer, J. Gerber, H. Eiffert, M. Prinz, and R. Nau Minocycline delays but does not attenuate the course of experimental autoimmune encephalomyelitis in Streptococcus pneumoniae-infected mice J. Antimicrob. Chemother., January 1, 2007; 59(1): 74 - 79. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. A. Babcock, M. Wirenfeldt, T. Holm, H. H. Nielsen, L. Dissing-Olesen, H. Toft-Hansen, J. M. Millward, R. Landmann, S. Rivest, B. Finsen, et al. Toll-Like Receptor 2 Signaling in Response to Brain Injury: An Innate Bridge to Neuroinflammation J. Neurosci., December 6, 2006; 26(49): 12826 - 12837. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Visser, M.-J. Melief, D. van Riel, M. van Meurs, E. A. Sick, S. Inamura, J. J. Bajramovic, S. Amor, R. Q. Hintzen, L. A. Boven, et al. Phagocytes Containing a Disease-Promoting Toll-Like Receptor/Nod Ligand Are Present in the Brain during Demyelinating Disease in Primates Am. J. Pathol., November 1, 2006; 169(5): 1671 - 1685. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Herrmann, M. Kellert, H. Schmidt, A. Mildner, U. K. Hanisch, W. Bruck, M. Prinz, and R. Nau Streptococcus pneumoniae Infection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2. Infect. Immun., August 1, 2006; 74(8): 4841 - 4848. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. S. Jack, N. Arbour, J. Manusow, V. Montgrain, M. Blain, E. McCrea, A. Shapiro, and J. P. Antel TLR Signaling Tailors Innate Immune Responses in Human Microglia and Astrocytes J. Immunol., October 1, 2005; 175(7): 4320 - 4330. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Visser, H. Jan de Heer, L. A. Boven, D. van Riel, M. van Meurs, M.-J. Melief, U. Zahringer, J. van Strijp, B. N. Lambrecht, E. E. Nieuwenhuis, et al. Proinflammatory Bacterial Peptidoglycan as a Cofactor for the Development of Central Nervous System Autoimmune Disease J. Immunol., January 15, 2005; 174(2): 808 - 816. [Abstract] [Full Text] [PDF] |
||||






