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Infection and Immunity, October 2003, p. 5541-5548, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5541-5548.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Pneumococcal Lipoteichoic Acid (LTA) Is Not as Potent as Staphylococcal LTA in Stimulating Toll-Like Receptor 2

Seung Hyun Han,1 Je Hak Kim,1 Michael Martin,2 Suzanne M. Michalek,2 and Moon H. Nahm1,2*

Departments of Pathology,1 Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 352942

Received 24 April 2003/ Returned for modification 24 June 2003/ Accepted 8 July 2003

Streptococcus pneumoniae is a leading cause of gram-positive sepsis, and lipoteichoic acid (LTA) may be important in causing gram-positive bacterial septic shock. Even though pneumococcal LTA is structurally distinct from the LTA of other gram-positive bacteria, the immunological properties of pneumococcal LTA have not been well characterized. We have investigated the ability of LTAs to stimulate human monocytes by using highly pure and structurally intact preparations of pneumococcal LTA and its two structural variants. The variants were pneumococcal LTA with only one acyl chain (LTA-1) and completely deacylated LTA (LTA-0). The target cells used in the study were peripheral blood mononuclear cells (PBMCs) and two model cell lines (CHO/CD14/TLR2 and CHO/CD14/TLR4) that express human CD25 protein in response to Toll-like receptor 2 (TLR2) and TLR4 stimulation, respectively. Intact pneumococcal LTA and LTA-1 stimulated PBMC and CHO/CD14/TLR2 cells in a dose-dependent manner but did not stimulate CHO/CD14/TLR4 cells. Pneumococcal LTA was about 100-fold less potent than Staphylococcus aureus LTA in stimulating the CHO/CD14/TLR2 cells and PBMCs. LTA-0 (or pneumococcal teichoic acid) stimulated neither CHO/CD14/TLR2 nor CHO/CD14/TLR4 cells even at high concentrations. Excess teichoic acid, LTA-0, antibodies to phosphocholine, or antibodies to TLR4 did not inhibit the LTA-induced TLR2 stimulation. However, antibodies to CD14, TLR1, or TLR2 suppressed tumor necrosis factor alpha (TNF-{alpha}) production by PBMCs in response to LTA or LTA-1. These results suggest that pneumococcal LTA with one or both acyl chains stimulates PBMCs primarily via TLR2 with the help of CD14 and TLR1.

* Corresponding author. Mailing address: University of Alabama at Birmingham, 845 19th St. South, BBRB 614 Birmingham, AL 35294. Phone: (205) 934-0163. Fax: (205) 975-2149. E-mail: Nahm{at}uab.edu.

Editor: A. D. O'Brien

Infection and Immunity, October 2003, p. 5541-5548, Vol. 71, No. 10
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.10.5541-5548.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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