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Infection and Immunity, July 2003, p. 3707-3713, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.3707-3713.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Teichoic Acids Are Not Required for Streptococcus pneumoniae and Staphylococcus aureus Cell Walls To Trigger the Release of Tumor Necrosis Factor by Peripheral Blood Monocytes

P. A. Majcherczyk,1 E. Rubli,1 D. Heumann,2 M. P. Glauser,2 and P. Moreillon1*

Institute of Fundamental Microbiology, University of Lausanne, 1015 Lausanne,1 Division of Infectious Diseases, Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland2

Received 22 January 2003/ Returned for modification 27 February 2003/ Accepted 9 April 2003

In gram-negative bacteria, the outer membrane lipopolysaccharide is the main component triggering cytokine release from peripheral blood mononuclear cells (PBMCs). In gram-positive bacteria, purified walls also induce cytokine release, but stimulation requires 100 times more material. Gram-positive walls are complex megamolecules reassembling distinct structures. Only some of them might be inflammatory, whereas others are not. Teichoic acids (TA) are an important portion (≥50%) of gram-positive walls. TA directly interact with C3b of complement and the cellular receptor for platelet-activating factor. However, their contribution to wall-induced cytokine-release by PBMCs has not been studied in much detail. In contrast, their membrane-bound lipoteichoic acids (LTA) counterparts were shown to trigger inflammation and synergize with peptidoglycan (PGN) for releasing nitric oxide (NO). This raised the question as to whether TA are also inflammatory. We determined the release of tumor necrosis factor (TNF) by PBMCs exposed to a variety of TA-rich and TA-free wall fragments from Streptocccus pneumoniae and Staphylococcus aureus. TA-rich walls from both organisms induced measurable TNF release at concentrations of 1 µg/ml. Removal of wall-attached TA did not alter this activity. Moreover, purified pneumococcal and staphylococcal TA did not trigger TNF release at concentrations as high as ≥100 µg/ml. In contrast, purified LTA triggered TNF release at 1 µg/ml. PGN-stem peptide oligomers lacking TA or amino-sugars were highly active and triggered TNF release at concentrations as low as 0.01 µg/ml (P. A. Majcherczyk, H. Langen, et al., J. Biol. Chem. 274:12537-12543,1999). Thus, although TA is an important part of gram-positive walls, it did not participate to the TNF-releasing activity of PGN.

* Corresponding author. Mailing address: Institute of Fundamental Microbiology, University of Lausanne, 1015 Lausanne, Switzerland. Phone: 41-21-692-5601. Fax: 41-21-692-5605. E-mail: Philippe.Moreillon{at}imf.unil.ch.

Editor: J. N. Weiser

Infection and Immunity, July 2003, p. 3707-3713, Vol. 71, No. 7
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.7.3707-3713.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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