Dysregulation of monocyte oxidative burst in streptococcal endocarditis

Citation
E. Presterl et al., Dysregulation of monocyte oxidative burst in streptococcal endocarditis, EUR J CL IN, 31(10), 2001, pp. 902-906
Citations number
14
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
ISSN journal
00142972 → ACNP
Volume
31
Issue
10
Year of publication
2001
Pages
902 - 906
Database
ISI
SICI code
0014-2972(2001)31:10<902:DOMOBI>2.0.ZU;2-4
Abstract
Background Streptococcal subacute endocarditis is characterized by low-grad e systemic inflammation. Although structural cardiac defects are pivotal, p hagocytic cells, i.e. monocytes and neutrophils, are involved in the induct ion and the course of bacterial endocarditis. Decreased production of react ive oxygen metabolites was described in long-lasting infections. We hypothe sized that the oxidative burst of phagocytes induced by the infecting organ ism is defective in patients with streptococcal endocarditis. Patients and methods The monocytes and neutrophils of 11 patients with stre ptococcal native valve endocarditis were challenged with the respective pat hogens and two control streptococcal strains, and the oxidative burst was d etermined 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. Af ter cure the monocyte response to the pathogens was not different to the re sponse to the control strains. The monocyte response of the healthy volunte ers did not show any differences between the patients' pathogens and the co ntrol strains. The neutrophil oxidative burst to the pathogens was similar to that to the control streptococci in both patient and the volunteer group . Conclusions The decreased response of patient monocytes to the pathogens ma y contribute to the low-grade inflammatory response and to the course of st reptococcal endocarditis.