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Morphine induces sepsis in mice
M E Hilburger1, M W Adler, A L Truant
1Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
Abstract:
Gram-negative sepsis and subsequent endotoxic shock remain major health problems in the United States. The present study examined the role of morphine in inducing sepsis. Mice administered morphine by the subcutaneous implantation of a slow-release pellet developed colonization of the liver, spleen, and peritoneal cavity with gram-negative and other enteric bacteria. In addition, the mice became hypersusceptible to sublethal endotoxin challenge. The effects were blocked by the simultaneous implantation of a pellet containing the opioid antagonist naltrexone. These findings show that morphine pellet implantation in mice results in the escape of gram-negative organisms from the gastrointestinal tract, leading to the hypothesis that morphine used postoperatively or chronically for analgesia may serve as a cofactor in the precipitation of sepsis and shock. In addition, morphine-induced sepsis may provide a physiologically relevant model of gram-negative sepsis and endotoxic shock.
Insights
Morphine administration in mice led to bacterial spread and increased susceptibility to endotoxic shock. Naltrexone blocked these effects, suggesting morphine may contribute to sepsis development in patients.
Area of Science:
- Immunology
- Microbiology
- Pharmacology
Background:
- Gram-negative sepsis and endotoxic shock are significant health concerns.
- The potential role of morphine in sepsis development requires investigation.
Purpose of the Study:
- To investigate the effect of morphine on inducing sepsis in a mouse model.
- To explore the potential of morphine as a cofactor in sepsis and endotoxic shock.
Main Methods:
- Subcutaneous implantation of slow-release morphine pellets in mice.
- Assessment of bacterial colonization in liver, spleen, and peritoneal cavity.
- Evaluation of susceptibility to endotoxin challenge.
- Administration of naltrexone to block morphine's effects.
Main Results:
- Morphine pellet implantation caused gram-negative bacterial colonization in multiple organs.
- Mice treated with morphine exhibited increased susceptibility to endotoxin.
- Naltrexone co-administration prevented morphine-induced bacterial spread and hypersusceptibility.
Conclusions:
- Morphine administration facilitates the escape of gram-negative bacteria from the GI tract.
- Morphine may act as a cofactor in the development of sepsis and endotoxic shock.
- Morphine-induced sepsis offers a relevant model for studying gram-negative sepsis and endotoxic shock.