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Infection and Immunity, July 2003, p. 3901-3908, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.3901-3908.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Activation of Toll-Like Receptor 2 (TLR2) and TLR4/MD2 by Neisseria Is Independent of Capsule and Lipooligosaccharide (LOS) Sialylation but Varies Widely among LOS from Different Strains

Alison C. Pridmore,1 Gary A. Jarvis,2,3 Constance M. John,2,{dagger} Dominic L. Jack,1 Steven K. Dower,1 and Robert C. Read1*

Division of Genomic Medicine, Royal Hallamshire Hospital, University of Sheffield, Sheffield S10 2RX, United Kingdom,1 Department of Laboratory Medicine, University of California, San Francisco, California 94143,2 Center for Immunochemistry and VA Medical Center, San Francisco, California 941213

Received 30 January 2003/ Returned for modification 21 March 2003/ Accepted 26 April 2003

Lipooligosaccharide (LOS) structure and capsular polysaccharide of Neisseria meningitidis each greatly influence the virulence of the organism and the quality of host innate immune responses. In this study, we found that production of the proinflammatory cytokine tumor necrosis factor (TNF) by a human monocyte-derived cell line (THP-1) exposed to strains of N. meningitidis lacking capsule and/or with truncated LOS was similar to that elicited by the isogenic wild-type strain. These mutants also exhibited no difference in induction of the interleukin-8 (IL-8) promoter in a transfected HeLa cell system of Toll-like receptor 2 (TLR2) and TLR4/MD2 signaling. However, purified LOS from diverse strains of Neisseria (both N. meningitidis and N. gonorrhoeae) caused widely variant levels of IL-8 promoter induction in cells expressing MD2 that correlated with the production of TNF from THP-1 cells. These data suggest that although modification of the oligosaccharide chain of LOS and/or absence of capsule do not affect cell signaling mediated by TLR4/MD2, fine-structural differences in the LOS do influence signaling through TLR4/MD2 and, through this pathway, influence some of the proinflammatory responses elicited by Neisseria.

* Corresponding author. Mailing address: Division of Genomic Medicine, Royal Hallamshire Hospital, University of Sheffield, Sheffield S10 2RX, United Kingdom. Phone: 44 0 114 272 4072. Fax: 44 0 114 273 9926. E-mail: r.c.read{at}shef.ac.uk.

Editor: J. D. Clements

{dagger} Present address: MandalMed, San Francisco, CA 94132.

Infection and Immunity, July 2003, p. 3901-3908, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.3901-3908.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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