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The origin of the synergistic effect of muramyl dipeptide with endotoxin and peptidoglycan
Margreet A Wolfert1, Thomas F Murray, Geert-Jan Boons
1Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, Georgia 30602, USA. mwolfert@vet.uga.edu
Abstract:
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-alpha (TNF-alpha) secretion. Although incubation of cells with MDP alone produced minimal TNF-alpha, it caused significant expression of TNF-alpha mRNA. These findings suggest that the majority of TNF-alpha 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-alpha 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-alpha 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-alpha 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.
Insights
Muramyldipeptide (MDP) synergizes with bacterial components like LPS and PGN to boost tumor necrosis factor-alpha (TNF-alpha) production by removing a translation block. This suggests new therapeutic targets for mixed bacterial infections.
Area of Science:
- Immunology
- Microbiology
- Molecular Biology
Background:
- Mixed bacterial infections contribute to high patient mortality.
- Synergistic effects between bacterial components like muramyldipeptide (MDP) and lipopolysaccharide (LPS) may drive inflammation.
- Mononuclear phagocytes play a key role in inflammatory responses to bacterial stimuli.
Purpose of the Study:
- To investigate the synergistic effect of MDP with LPS or peptidoglycan (PGN) on pro-inflammatory cytokine production.
- To elucidate the mechanisms underlying the synergistic TNF-alpha response.
- To identify the receptors involved in MDP-mediated signaling.
Main Methods:
- Co-incubation of human Mono Mac 6 cells with MDP, LPS, and PGN.
- Measurement of tumor necrosis factor-alpha (TNF-alpha) secretion and mRNA expression.
- Assessment of the role of CD14, Toll-like receptor 2 (TLR2), and Toll-like receptor 4 (TLR4).
Main Results:
- MDP alone induced TNF-alpha mRNA but minimal protein, suggesting translational control.
- Co-incubation with LPS or PGN potentiated TNF-alpha secretion, appearing synergistic.
- The synergistic effect was attributed to the removal of a translational block on MDP-induced TNF-alpha mRNA.
- MDP's effects were independent of CD14, TLR2, and TLR4, indicating alternative receptor pathways.
Conclusions:
- MDP enhances TNF-alpha production by overcoming translational inhibition, particularly when combined with LPS or PGN.
- The signaling pathways for MDP differ from those primarily activated by LPS and PGN.
- Targeting these distinct mechanisms may be crucial for treating mixed bacterial infections.
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