Serotonin syndrome due to co-administration of linezolid and venlafaxine.

$ 50%, and glatiramer did not modify this effect. When infected cells were exposed to ampicillin for 24 h after phagocytosis, the bacterial load was reduced by $ 1.7 log compared with the original, post-phagocytosis inoculum. Glatira-mer, IFN-g, or the combination of glatiramer and IFN-g did not significantly modify this effect of ampicillin. In the next series of experiments, we examined the activity of moxifloxacin (4 mg/L) using the 5 h model. We observed a decrease in the post-phagocytosis inoculum of 1.34 ± 0.03, 1.26 ± 0.16, 1.31 ± 0.07 and 1.32 ± 0.07 log 10 units for cells treated with mox-ifloxacin alone, glatiramer and moxifloxacin, IFN-g and moxi-floxacin, and the combination of glatiramer, IFN-g and moxifloxacin, respectively. In parallel experiments, we examined the influence of glatiramer on the accumulation of moxifloxacin and no effect was seen [apparent cellular to extracellular drug concentration ratios at 2 h of 9.6 ± 2.0 in controls versus 9.4 ± 1.1 in cells exposed to glatiramer (20 mg/L) during the uptake period; similar values were found for cells pre-exposed to glatir-amer (20 mg/L) for 24 h]. Glatiramer did not influence the accumulation of three other quinolones (ciprofloxacin, levofloxa-cin and garenoxacin). Our data, therefore, show that the production of TNF-a is not critical in IFN-g-stimulated THP-1 cells for anti-Listeria activity. The model used has been validated to analyse the behaviour of intracellular L. monocytogenes with respect to the action of cytokines 5,6 and to the influence of antibiotics. THP-1 cells display functional receptors for TNF-a 7 and their presence in the cell line used here has been confirmed (J. Zanon, unpublished data). TNF-a may be more a potentializer of IFN-g 8 than a true effector for the control of L. monocytogenes growth in THP-1 cells. Because intracellular multiplication of L. monocytogenes is an important determinant in the persistence and the spread of the infection, our results suggest that glatiramer (i) may actually not increase this risk, and (ii) may not adversely affect ampicillin or quinolone-based antibiotic treatments should the necessity arise. This will need to be confirmed by in vivo studies. Acknowledgements Mrs N. Aguilera provided critical help in some of the experiments described in this paper and Ms M. C. Cambier maintained the cell culture line. S. C. was Boursier of the Belgian Fonds pour la Formation a ` la Recherche dans l'Industrie et l'Agriculture (F. (2003). Listeria monocytogenes infection as a complication of …