This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Glickstein, L. Articles by Steere, A. C. Search for Related Content PubMed PubMed Citation Articles by Glickstein, L. Articles by Steere, A. C.

 Previous Article  |  Next Article 

Infection and Immunity, October 2003, p. 6051-6053, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.6051-6053.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Inflammatory Cytokine Production Predominates in Early Lyme Disease in Patients with Erythema Migrans

Lisa Glickstein,^* Brian Moore, Tara Bledsoe, Nitin Damle, Vijay Sikand,^|| and Allen C. Steere^#

Division of Rheumatology/Immunology, New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02111

Received 11 April 2003/ Returned for modification 5 June 2003/ Accepted 13 July 2003

In a study of cytokine production ex vivo by Borrelia burgdorferi-stimulated peripheral blood mononuclear cells from 27 patients with culture-positive erythema migrans, production of inflammatory cytokines predominated, particularly gamma interferon and, to a lesser degree, tumor necrosis factor alpha. In contrast, with the exception of interleukin-13, anti-inflammatory cytokine production was negligible. Thus, B. burgdorferi antigens in early Lyme disease often induce a strong inflammatory response.

Editor: W. A. Petri, Jr.

Present address: Program in Biomedical Sciences, University of Michigan, Ann Arbor, MI 48109.

Present address: Biology Department, Tufts University, Medford, MA 02155.

Present address: 481 Kingstown Rd., Wakefield, RI 02879.

^|| Present address: 324 Flanders Rd., East Lyme, CT 06333.

^# Present address: Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114.

This article has been cited by other articles:

• Wang, G., Petzke, M. M., Iyer, R., Wu, H., Schwartz, I. (2008). Pattern of Proinflammatory Cytokine Induction in RAW264.7 Mouse Macrophages Is Identical for Virulent and Attenuated Borrelia burgdorferi. J. Immunol. 180: 8306-8315 [Abstract] [Full Text]  
• Behera, A. K., Hildebrand, E., Uematsu, S., Akira, S., Coburn, J., Hu, L. T. (2006). Identification of a TLR-Independent Pathway for Borrelia burgdorferi-Induced Expression of Matrix Metalloproteinases and Inflammatory Mediators through Binding to Integrin {alpha}3beta1. J. Immunol. 177: 657-664 [Abstract] [Full Text]