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Antimicrobial Agents and Chemotherapy, March 1999, p. 616-622, Vol. 43, No. 3
The Second Department of Internal Medicine,
Oita Medical University, Hasama, Oita, 879-5593, Japan
Received 7 July 1998/Returned for modification 9 November
1998/Accepted 29 December 1998
Treatment of septicemia caused by Escherichia coli with
ceftazidime (CAZ) may be associated with the development of
septic shock due to the release of bacterial lipopolysaccharide. We
examined the suppressive effect of clindamycin (CLDM) on CAZ-induced
release of endotoxin by cultured E. coli and the
subsequent production of inflammatory cytokines (tumor necrosis factor
alpha [TNF-
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Clindamycin Suppresses Endotoxin Released by Ceftazidime-Treated
Escherichia coli O55:B5 and Subsequent Production of
Tumor Necrosis Factor Alpha and Interleukin-1
] and interleukin-1
[IL-1]). E. coli ATCC 12014 was incubated in inactivated horse serum with or
without CLDM for 1, 4, or 18 h, followed by the addition of CAZ
and collection of the culture supernatant at 0, 1, and 2 h. The
concentration of endotoxin in each sample was measured by a chromogenic
Limulus test. Another portion of the culture
supernatant was added to THP-1 cell culture and incubated
for 4 h, and the concentrations of TNF- and IL-1 in the
supernatant were measured by an enzyme-linked immunosorbent assay. In
the control group (no CLDM), CAZ administration resulted in significant
increases in endotoxin, TNF-, and IL-1 concentrations. Pretreatment of E. coli with CLDM for 4 or 18 h
before the addition of CAZ significantly suppressed the concentrations
of endotoxin, TNF-, and IL-1 in a time-dependent manner. In
addition, CAZ treatment transformed E. coli from
rod-shaped bacteria to filament-like structures, as determined by
electron microscopy, while pretreatment with CLDM prevented these
morphological changes. Our in vitro studies showed that CAZ-induced
release of large quantities of endotoxin by E. coli
could be suppressed by prior administration of CLDM.
*
Corresponding author. Mailing address: The Second
Department of Internal Medicine, Oita Medical University, Hasama,
Oita, 879-5593, Japan. Phone: 81-97-586-5804. Fax: 81-97-549-4245. E-mail: mnasu{at}oita-med.ac.jp.
Antimicrobial Agents and Chemotherapy, March 1999, p. 616-622, Vol. 43, No. 3
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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