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and MnSOD by endotoxin: role of
membrane CD14 and Toll-like receptor-4
1 Research Service, Stratton Veterans Affairs Medical Center, and 2 Department of Medicine and Center for Cardiovascular Biology, Albany Medical College, Albany 12208; and 3 Division of Molecular Medicine, North Shore University Hospital, New York University School of Medicine, Manhasset, New York 11030
Endotoxin (LPS) is a potent inducer of
tumor necrosis factor-
(TNF-) and manganese superoxide dismutase
(MnSOD). Recent evidence suggests that LPS induction of TNF- and
MnSOD mRNAs is mediated through distinct intracellular signal
transduction pathways. Membrane CD14 (mCD14) and Toll-like receptor-4
(TLR4) mediate LPS induction of TNF- in macrophages. In the current study, we evaluated the role of mCD14 and TLR4 in LPS induction of
MnSOD using peritoneal macrophages from CD14 knockout (CD14-KO) mice
and mice with the Tlr4 gene point mutation (C3H/HeJ) or
deletion (C57BL/10ScCr). We studied mCD14-dependent (1 and 10 ng/ml)
and mCD14-independent (1,000 ng/ml) concentrations of LPS. Compared with control (BALB/c) macrophages, LPS at 1 and 10 ng/ml failed to
induce TNF- or MnSOD mRNA in CD14-KO macrophages. However, LPS at
1,000 ng/ml induced TNF- and MnSOD mRNAs equally in macrophages from
CD14-KO and control mice. LPS (1, 10, or 1,000 ng/ml) failed to induce
TNF- or MnSOD mRNA and failed to activate nuclear factor-
B in
C3H/HeJ or C57BL/10ScCr macrophages. Measurements of TNF- and MnSOD
enzyme activity paralleled TNF- and MnSOD mRNA levels. These data
demonstrate that, like TNF-, induction of MnSOD by LPS is mediated
by mCD14 and TLR4 in murine macrophages.
tumor necrosis factor-; manganese superoxide dismutase; endotoxin resistance; nuclear factor-B; peritoneal macrophage
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