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Production1
North Shore University Hospital/New York University School of Medicine, Manhasset, NY 11030
Recent in vitro studies have suggested that CD14, a major receptor
for LPS, may also be a receptor for cell wall components of
Gram-positive bacteria and thus play a role in Gram-positive shock. To
analyze the in vivo role of CD14 in responses to Gram-positive
bacteria, CD14-deficient and control mice were injected with
Staphylococcus aureus, and the effects on lethality,
bacterial clearance, and production of cytokines were analyzed.
Survival of CD14-deficient and control mice did not differ
significantly after administration of various doses of either
unencapsulated or encapsulated S. aureus; furthermore,
mice in both groups displayed similar symptoms of shock. In addition,
inflammatory cytokines such as TNF-
and IL-6 were readily detectable
in the serum of CD14-deficient mice injected with live or
antibiotic-killed S. aureus. Surprisingly, the serum
concentration of TNF- in CD14-deficient mice was at least threefold
higher than in control mice after injection of either unencapsulated or
encapsulated S. aureus, suggesting that CD14
down-regulates TNF-. A similar increase in serum TNF- occurred
when CD14-deficient animals were injected with gentamicin-killed
bacteria even though no symptoms of shock were observed. These studies
indicate that CD14, in contrast to its key function in responses to the
Gram-negative bacterium, Escherichia coli 0111, does not
play a prominent role in septic shock induced by S.
aureus, and that the symptoms of S. aureus shock
are not due solely to TNF-.
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