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* Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605;
Department of Pediatrics, Freie Universität Berlin, Berlin, Germany;
Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
Channing Laboratory, Brigham and Women’s Hospital, and Departments of Medicine, Microbiology, and Molecular Genetics, Harvard Medical School, Boston, MA 02115;
¶ Evans Biomedical Research Center, Boston University School of Medicine, Boston, MA 02118;
|| Lipid Metabolism Unit, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114;
# Department of Pathology, Harvard Medical School, Boston, MA 02115; and
** Department of Pediatrics, University of California at San Diego, La Jolla, CA 92093
Group B streptococci (GBS) vigorously activate inflammatory
responses. We reported previously that a secreted GBS "factor"
activates phagocytes via Toll-like receptor (TLR)2 and TLR6, but that
GBS cell walls activate cells independently of these receptors. We
hypothesized that the phagocytic immune functions in response to GBS,
such as inflammation, uptake, and elimination of bacteria, occur
through a coordinated engagement of TLRs, along with the coreceptors
CD14 and CD11b/CD18. Using various knockout mice we show that
GBS-induced activation of p38 and NF-
B depends upon the expression
of the cytoplasmic TLR adapter protein, myeloid differentiation factor
88 (MyD88), but not TLR2 and/or TLR4. Macrophages with deletions of
CD14 and complement receptor 3 had a normal cytokine response to whole
bacteria, although the response to GBS factor was abrogated in
CD14-null cells. The intracellular formation of bactericidal oxygen
species proved to be MyD88 dependent; however, uptake of GBS, a
prerequisite for intracellular killing by O2 radicals,
occurred independently of MyD88. While deletion of complement receptor
3 greatly diminished the uptake of opsonized GBS, it did not affect the
formation of bactericidal O2 radicals or inflammatory
signaling intermediates. We conclude that the inflammatory,
bactericidal, and phagocytic responses to GBS occur via parallel but
independent processes.
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