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B Activation and TNF Production Induced by Lipopolysaccharide and Group B Streptococcal Cell Walls1
*
Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;
Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, Trondheim, Norway;
The Maxwell Finland Laboratory for Infectious Diseases, Division of Infectious Diseases, Department of Medicine, Boston Medical Center and Boston University School of Medicine, Boston, MA 02118;
§
Institute of Microbiology, Faculty of Medicine and Surgery, University of Messina, Messina, Italy
This study was undertaken to evaluate the role of CD14 and
complement receptors type 3 (CR3) and 4 (CR4) in mediating TNF release
and NF-
B activation induced by LPS and cell wall preparations from
group B streptococci type III (GBS). LPS and GBS caused TNF secretion
from human monocytes in a CD14-dependent manner, and soluble CD14, LPS
binding protein, or their combination potentiated both LPS- and
GBS-induced activities. Blocking of either CD14 or CD18, the common
ß-subunit of CR3 and CR4, decreased GBS-induced TNF release, while
LPS-mediated TNF production was inhibited by anti-CD14 mAb only.
Chinese hamster ovary cell transfectants (CHO) that express human CD14
(CHO/CD14) responded to both LPS and GBS with NF-B translocation,
which was inhibited by anti-CD14 mAb and enhanced by LPS binding
protein. While LPS showed fast kinetics of NF-B activation in
CHO/CD14 cells, a slower NF-B response was induced by GBS. LPS also
activated NF-B in CHO cells transfected with either human CR3 or CR4
cDNA, although responses were delayed and weaker than those of CHO/CD14
cells. In contrast to LPS, GBS failed to induce NF-B in CHO/CR3 or
CHO/CR4 cells. Both C3H/OuJ (Lpsn) and
C3H/HeJ (Lpsd) mouse peritoneal macrophages
responded to GBS with TNF production and NF-B translocation, whereas
LPS was active only in C3H/OuJ macrophages. Thus, LPS and GBS
differentially involve CD14 and CR3 or CR4 for signaling NF-B
activation in CHO cells and TNF release in human monocytes, and engage
a different set of receptors and/or intracellular signaling pathways in
mouse macrophages.
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