Original scientific paper

https://doi.org/10.2478/v10007011-0024-4

Tigecycline attenuates polymorphonuclear leukocyte (PMN) receptors but not functions

ARE NAESS ; Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021Bergen, Norway
HRISTINA ANDREEVA orcid.org/0000-0002-2469-3636 ; Department of Immunology and Transfusion Medicine, University of Tromsoe, Tromsoe University Hospital, N-9038 Tromsoe, Norway
STEINAR SØRNES ; Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021Bergen, Norway

Abstract

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 Fcγ- 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 Fcγ 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) Fcγ receptors. Although statistically significant, the differences were small and did not influence the PMN function as measured by phagocytosis and oxidative burst.

Keywords

tigecycline; leukocyte; phagocytosis; oxidative burst

Hrčak ID:

69441

URI

https://hrcak.srce.hr/69441

Publication date:

1.9.2011.

Article data in other languages: croatian

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