JAC Advance Access published online on January 16, 2004
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkh056
© 2004 by The British Society for Antimicrobial Chemotherapy
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Original article
1 Department of Infectious
Diseases, Malmö University Hospital, Lund University,
SE 205 02 Malmö, Sweden
* Corresponding author. E-mail: Peter.Lanbeck{at}inf.mas.lu.se.
Received 21 August 2003
; revised 28 October 2003
; accepted 5 November 2003
Objectives: Antimicrobial agents are
important risk factors for infusion phlebitis, but the risk varies
between different antibiotics. Erythromycin and dicloxacillin are
known to induce phlebitis frequently, as well as to exert toxic
effects on cultured endothelial cells. The pathogenesis of infusion
phlebitis is unclear, but chemical toxicity is thought to lead to
inflammation and subsequent thrombosis. In the present study, endothelial cells
were exposed to antibiotics at the range of concentrations used
for intravenous administration, followed by analysis of pro-inflammatory
and pro-coagulant surface molecules. Methods: Primary human umbilical vein endothelial
cells (HUVEC) and the endothelial hybrid cell line EaHy926 were
exposed to dicloxacillin, erythromycin, benzylpenicillin and cefuroxime
(all at 6250 mg/L) for 60 min, followed by washing. After 5 or 24
h additional incubation, cells were analysed for E-selectin (CD62E),
tissue factor (TF) or intercellular adhesion molecule 1 (ICAM-1,
CD54) density by flow cytometry. Results: Despite constitutive expression of
ICAM-1 (34%) in HUVEC, 6250 mg/L of dicloxacillin or erythromycin
significantly increased the number of cells with ICAM-1 expression
by 37% and 30%, respectively. In contrast, cefuroxime
and benzylpenicillin did not up-regulate ICAM-1 above background
levels. A similar pattern was seen with the endothelial cell line
EaHy926. The E-selectin and TF density were not affected by the
antibiotics examined. Conclusions: The results of this study support
the theory that endothelial cells that are affected by high concentrations
of antibiotics may initiate an inflammatory response through expression
of ICAM-1. This is a novel finding in the pathogenesis of infusion
phlebitis.
Keywords: phlebitis/chemically induced, antibiotics, adhesion
molecules, CD54
Dicloxacillin and erythromycin at high concentrations
increase
ICAM-1 expression by endothelial cells: a possible factor in the pathogenesis
of infusion phlebitis
2 Department of Medical Microbiology,
Malmö University Hospital, Lund University,
SE 205 02 Malmö, Sweden
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