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Infection and Immunity, April 2000, p. 2167-2170, Vol. 68, No. 4
Department of Infectology and Pediatric
Immunology, Medical and Health Science Center, University of
Debrecen, Debrecen, Hungary
Received 4 October 1999/Returned for modification 30 November
1999/Accepted 14 January 2000
Phagocytic and killing capacities of resident and
cytokine-activated human macrophages against group B
Streptococcus (GBS) type III were studied. Evidence is
presented that monocyte-derived macrophages from cord and adults ingest
serum-opsonized GBS but that killing of bacteria was negligible in
resident cells. Treatment of adult macrophages with recombinant human
gamma interferon (rhIFN-
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Survival of Group B Streptococcus Type
III in Mononuclear Phagocytes: Differential Regulation of Bacterial
Killing in Cord Macrophages by Human Recombinant Gamma Interferon and
Granulocyte-Macrophage Colony-Stimulating Factor
; 100 U/ml) or recombinant human
granulocyte-macrophage colony-stimulating factor (rhGM-CSF; 200 U/ml)
resulted in significant increases of killing of GBS (P < 0.01 for each). The killing capacity of cord macrophages treated
with rhGM-CSF was also enhanced compared to that of untreated cells
(P < 0.01). However, treatment with rhIFN-
resulted in only a moderate increase in the capacity of cord
macrophages to kill GBS (P > 0.1). These results
mirrored the effect of rhIFN-
on candidacidal capacities of cord and
adult macrophages, reported earlier from our laboratory. These data indicate differential modulation of neonatal macrophages by rhGM-CSF and rhIFN-
. We suggest that administration of rhGM-CSF to neonates with invasive GBS disease may enhance host resistance to these bacteria.
*
Corresponding author. Mailing address: Department of
Infectology and Pediatric Immunology, Medical and Health Science
Center, University of Debrecen, POB:32, H-4012 Debrecen, Hungary.
Phone: (36) (52) 416 841. Fax: (36) (52) 430-323. E-mail:
LMarodi{at}jaguar.dote.hu.
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