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*
Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605;
Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
Eijkman Winkler Institute of Medical and Clinical Microbiology, University of Utrecht, Utrecht, The Netherlands;
Channing Laboratory, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115;
¶ Boston University School of Medicine, Boston, MA 02118;
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Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, Trondheim, Norway;
#
Department of Pediatrics, University of California at San Diego, La Jolla, CA 92093; and
**
Department of Pediatrics, Free University, Berlin, Germany.
Group B streptococcus (GBS) imposes a major health threat to
newborn infants. Little is known about the molecular basis of
GBS-induced sepsis. Both heat-inactivated whole GBS bacteria and a
heat-labile soluble factor released by GBS during growth (GBS-F) induce
nuclear translocation of NF-
B, the secretion of TNF-
, and the
formation of NO in mouse macrophages. Macrophages from mice with a
targeted disruption of MyD88 failed to secrete TNF- in response to
both heat-inactivated whole bacteria and GBS-F, suggesting that
Toll-like receptors (TLRs) are involved in different aspects of GBS
recognition. Immune cell activation by whole bacteria differed
profoundly from that by secreted GBS-F. Whole GBS activated macrophages
independently of TLR2 and TLR6, whereas a response to the secreted
GBS-F was not observed in macrophages from TLR2-deficient animals. In
addition to TLR2, TLR6 and CD14 expression were essential for GBS-F
responses, whereas TLR1 and TLR4 or MD-2 did not appear to be involved.
Heat lability distinguished GBS-F from peptidoglycan and lipoproteins.
GBS mutants deficient in capsular polysaccharide or 
-hemolysin had
GBS-F activity comparable to that of wild-type streptococci. We
suggest that CD14 and TLR2 and TLR6 function as coreceptors for
secreted microbial products derived from GBS and that cell wall
components of GBS are recognized by TLRs distinct from TLR1, 2, 4, or
6.
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