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Tigecycline attenuates polymorphonuclear leukocyte (PMN) receptors but not functions

Are Naess1, Hristina Andreeva, Steinar Sørnes

  • 1Institute of Medicine, University of Bergen, Haukeland University Hospital, N-5021Bergen, Norway.

Acta Pharmaceutica (Zagreb, Croatia)
|September 28, 2011
PubMed

Insights

Tigecycline slightly reduced immune cell receptors at high doses but did not impact Staphylococcus aureus phagocytosis or oxidative burst in polymorphonuclear leukocytes (PMNs). This antibiotic maintains crucial immune cell functions.

Area of Science:

  • Immunology
  • Pharmacology
  • Microbiology

Background:

  • Tigecycline achieves high intracellular concentrations within polymorphonuclear leukocytes (PMNs).
  • Understanding tigecycline's impact on PMN function is crucial for its clinical application.
  • PMNs play a vital role in the innate immune response against bacterial infections.

Purpose of the Study:

  • To evaluate the effects of tigecycline on human PMN receptors and functions.
  • To assess if tigecycline influences phagocytosis and oxidative burst induced by Staphylococcus aureus.

Main Methods:

  • Human PMNs were incubated with varying concentrations of tigecycline (0.1 to 100 mg L-1).
  • Flow cytometry was used to measure PMN Fcγ receptors (CD16, CD32) and complement receptors (CD11b, CD35).
  • Phagocytosis and oxidative burst assays using Staphylococcus aureus were performed.

Main Results:

  • Tigecycline caused minor, concentration-dependent decreases in the density of complement receptors CD11b and CD35, and Fcγ receptors CD16 and CD32.
  • The percentage of receptor-bearing cells remained largely unaffected, except for a slight reduction in CD16 positive cells at high concentrations.
  • Tigecycline did not alter phagocytosis or oxidative burst activity of PMNs against Staphylococcus aureus.

Conclusions:

  • Tigecycline is associated with reduced PMN complement and Fcγ receptor density, particularly at high concentrations.
  • These minor changes in receptor density did not significantly impair PMN phagocytosis or oxidative burst functions.
  • Tigecycline appears to preserve key PMN functions essential for combating bacterial infections like those caused by Staphylococcus aureus.

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