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Antimicrobial Agents and Chemotherapy, December 1998, p. 3073-3078, Vol. 42, No. 12
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Antibiotic-Induced Release of Lipoteichoic Acid and Peptidoglycan from Staphylococcus aureus: Quantitative Measurements and Biological Reactivities

P. van Langevelde,1 J. T. van Dissel,1,* E. Ravensbergen,1 B. J. Appelmelk,2 I. A. Schrijver,3 and P. H. P. Groeneveld1

Department of Infectious Diseases, Leiden University Medical Center, Leiden,1 Department of Medical Microbiology, Free University, Amsterdam,2 and Department of Immunology, Erasmus University, Rotterdam,3 The Netherlands

Received 11 March 1998/Returned for modification 19 June 1998/Accepted 13 September 1998

Antibiotics with different mechanisms of action may vary with respect to their effects on the release and immunostimulatory activities of cell wall fragments from gram-positive bacteria. Therefore, after Staphylococcus aureus was cultured for 4 h in the absence of antibiotics (control) and in the presence of beta -lactam antibiotics (imipenem, flucloxacillin, or cefamandole) and protein synthesis-inhibiting antibiotics (erythromycin, clindamycin, or gentamicin), the lipoteichoic acid (LTA) and peptidoglycan (PG) levels in the bacterial supernatants were measured. beta -Lactam antibiotics greatly enhanced the release of LTA and PG (4- to 9-fold and 60- to 85-fold, respectively), whereas protein synthesis inhibitors did not affect PG release and even inhibited the release of LTA compared to the amount of LTA released in control cultures. The capacity of beta -lactam supernatants to stimulate the production of tumor necrosis factor alpha and interleukin-10 in human whole blood was significantly higher than that of protein synthesis inhibitor or control supernatants; the amounts of these cytokines released were directly proportional to the concentrations of PG and LTA in the supernatants. Enzymatic degradation of PG in the supernatants indicated that PG was mainly responsible for the observed biological reactivity.

* Corresponding author. Mailing address: Department of Infectious Diseases, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands. Phone: 31 71 526-2613. Fax: 31 71 526-6758. E-mail: J.van_Dissel{at}Thuisnet.LeidenUniv.NL.

Antimicrobial Agents and Chemotherapy, December 1998, p. 3073-3078, Vol. 42, No. 12
0066-4804/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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