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Infection and Immunity, July 2000, p. 3965-3970, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Peptidoglycan and Lipoteichoic Acid from Staphylococcus aureus Induce Tumor Necrosis Factor Alpha, Interleukin 6 (IL-6), and IL-10 Production in Both T Cells and Monocytes in a Human Whole Blood Model

J. E. Wang,1,* P. F. Jørgensen,1 M. Almlöf,1,2 C. Thiemermann,3 S. J. Foster,4 A. O. Aasen,1 and R. Solberg2

Institute for Surgical Research, Rikshospitalet-National Hospital, N-0027 Oslo,1 and Department of Pharmacology, School of Pharmacy, University of Oslo, N-0316 Oslo,2 Norway, and William Harvey Research Institute, St. Bartholomew's Hospital, Medical College, Charterhouse Square, London EC1M 6BQ,3 and Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield,4 United Kingdom

Received 27 January 2000/Returned for modification 25 March 2000/Accepted 23 April 2000

We have examined the ability of peptidoglycan (PepG) and lipoteichoic acid (LTA) isolated from Staphylococcus aureus to induce the release of tumor necrosis factor alpha (TNF-alpha ), interleukin-6 (IL-6), and IL-10 in whole human blood and identified the cellular origins of these cytokines. Both PepG and LTA induced transient increases in TNF-alpha and IL-10 in plasma, with peak values at 6 and 12 h, respectively. IL-6 values increased throughout the experimental period (24 h). The TNF-alpha , IL-6, and IL-10 release induced by PepG and LTA was dose dependent. Only PepG was a potent inducer of TNF-alpha secretion. After stimulation of whole blood with PepG or LTA, very pure populations of monocytes (CD14 positive), T cells (CD2 positive), B cells (CD19 positive), and granulocytes (CD15 positive) were isolated by immunomagnetic separation and analyzed by reverse transcription-PCR for mRNA transcripts encoding TNF-alpha , IL-6, and IL-10. The TNF-alpha mRNA results were inconclusive. In contrast, PepG induced IL-6 and IL-10 mRNA accumulation in both T cells and monocytes. LTA, as well as lipopolysaccharide, induced IL-6 and IL-10 mRNA production in monocytes and possibly in T cells. Whether granulocytes and B cells produce cytokines in response to bacterial stimuli remains obscure. Blockade of the CD14 receptors with monoclonal antibodies (18D11) had no influence on the PepG-induced release of TNF-alpha but attenuated the LTA-induced release of the same cytokine. In conclusion, our data indicate that circulating T cells and monocytes contribute to cytokine production in sepsis caused by gram-positive bacteria.

* Corresponding author. Mailing address: Institute for Surgical Research, Rikshospitalet-National Hospital, Sognsvannsveien 20, N-0027 Oslo, Norway. Phone: 47 23 07 35 20. Fax: 47 23 07 35 30. E-mail: jacob.wang{at}klinmed.uio.no.

Infection and Immunity, July 2000, p. 3965-3970, Vol. 68, No. 7
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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