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Dysregulation of monocyte oxidative burst in streptococcal endocarditis
E Presterl1, E Rokita, W Graninger
1Institute of Hygiene, Department of Clinical Microbiology, University of Vienna, Allgemeines Krankenhaus 5P, Währinger Gürtel 18-20, A-1090 Vienna, Austria. Alexander.Hirschl@akh-wien.ac.at
Background:
Streptococcal subacute endocarditis is characterized by low-grade systemic inflammation. Although structural cardiac defects are pivotal, phagocytic cells, i.e. monocytes and neutrophils, are involved in the induction and the course of bacterial endocarditis. Decreased production of reactive oxygen metabolites was described in long-lasting infections. We hypothesized that the oxidative burst of phagocytes induced by the infecting organism is defective in patients with streptococcal endocarditis.
Patients And Methods:
The monocytes and neutrophils of 11 patients with streptococcal native valve endocarditis were challenged with the respective pathogens and two control streptococcal strains, and the oxidative burst was determined by fluorescence-activated cell sorter analysis. These experiments were done before any antibiotic therapy was administered, and repeated at least 12 months after recovery. Eight volunteers served as healthy controls.
Results:
The monocyte response to the respective pathogens was decreased in the patient groups compared to the response to the control streptococci. After cure the monocyte response to the pathogens was not different to the response to the control strains. The monocyte response of the healthy volunteers did not show any differences between the patients' pathogens and the control strains. The neutrophil oxidative burst to the pathogens was similar to that to the control streptococci in both patient and the volunteer group.
Conclusion:
The decreased response of patient monocytes to the pathogens may contribute to the low-grade inflammatory response and to the course of streptococcal endocarditis.