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J. Biol. Chem., Vol. 277, Issue 42, 39179-39186, October 18, 2002
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From the Although the basis for the high mortality rate
for patients with mixed bacterial infections is likely to be
multifactorial, there is evidence for a synergistic effect of
muramyldipeptide (MDP) with lipopolysaccharide (LPS) on the synthesis
of proinflammatory cytokines by mononuclear phagocytes. In this study,
co-incubation of human Mono Mac 6 cells with MDP and either LPS or
peptidoglycan (PGN) resulted in an apparent synergistic effect on tumor
necrosis factor-
The Origin of the Synergistic Effect of Muramyl Dipeptide with
Endotoxin and Peptidoglycan*
§,
, and
Department of Large Animal Medicine, the
¶ Department of Physiology and Pharmacology, College of Veterinary
Medicine, and the Complex Carbohydrate Research Center,
University of Georgia, Athens, Georgia 30602
(TNF-) secretion. Although incubation of cells
with MDP alone produced minimal TNF-, it caused significant
expression of TNF- mRNA. These findings suggest that the
majority of TNF- mRNA induced by MDP alone is not translated
into protein. Furthermore, simultaneous incubation of cells with MDP
and either LPS or PGN resulted in TNF- mRNA expression that
approximated the sum of the amounts expressed in response to MDP, LPS,
and PGN individually. These findings indicate that the apparent
synergistic effect of MDP on TNF- production induced by either
LPS or PGN is due to removal of a block in translation of the mRNA
expressed in response to MDP. In subsequent studies, the effects of MDP
alone and its effect on the production of TNF- by LPS and PGN were
determined to be independent of CD14, Toll-like receptor 2, and
Toll-like receptor 4. These findings indicate that MDP acts through
receptor(s) other than those primarily responsible for transducing the
effects of LPS and PGN. Successful treatment of patients having mixed bacterial infections is likely to require interventions that address the mechanisms involved in responses induced by a variety of bacterial cell wall components.
*
This work was supported in part by Georgia Heart Association
Grant 0051229B and National Institutes of Health Grant GM61761-02.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
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