Tigecycline attenuates polymorphonuclear leukocyte (PMN) receptors but not functions
Type
Journal article; Peer reviewedPeer reviewed
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Date
2011
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Tigecycline achieves high intracellular concentrations in
polymorphonuclear leukocytes (PMNs). To evaluate the
effects of tigecycline on human PMNs, PMNs were incubated
with tigecycline dilutions (0.1 to 100 mg L–¹). Phagocytosis-
associated PMN Fcg- and complement receptors
as well as phagocytosis and oxidative burst induced by
Staphylococcus aureus were measured by flow cytometry.
Incubation with tigecycline caused small but significant
decreases in the density of complement receptors CD11b
and CD35 (all concentrations) and Fcg receptors CD16 and
CD32 (high concentrations), but not in the percentages of
receptor-bearing cells, except for small reductions in the
proportions of CD16 positive cells at high concentrations.
Tigecycline had no effect on phagocytosis or oxidative
burst induced by S. aureus. Tigecycline was thus associated
with decreased density of PMN complement and (at
high concentrations) Fcg receptors. Although statistically
significant, the differences were small and did not influence
the PMN function as measured by phagocytosis and
oxidative burst.