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Morphine modulation of peritoneal inflammation in Atlantic salmon and CB6 mice
M Chadzinska1, E Kolaczkowska, R Seljelid
1Department of Evolutionary Immunology, Institute of Zoology, Jagiellonian University, Krakow, Poland.
Abstract:
Peritoneal inflammation is a convenient model for comparisons of modulatory effects of morphine in phylogenetically distant vertebrates. Both in salmon and mice morphine injected intraperitoneally together with an irritant (thioglycollate) significantly inhibits inflammation as estimated by the number of peritoneal leukocytes. The low number of exudate cells in morphine-treated animals seems to be compensated by their high activity, as evidenced by the enhanced phorbol myristate acetate-induced respiratory burst. The morphine-inhibited influx of leukocytes into the irritated peritoneal cavity correlates with the morphine-lowered level of plasma chemotactic factors both in fish and mice. It implies that morphine impairs the level of plasma chemotactic factor either directly (affecting their release from the resident peritoneal cells) or indirectly (decreasing the number of inflammatory leukocytes by inhibition of their migration from hemopoietic sites). The inhibitory effects of morphine on both the cell number and chemoattractant level are completely reversed by the naltrexone pretreatment, which implicates the involvement of opioid receptors.
Insights
Morphine significantly reduces peritoneal inflammation in both salmon and mice by inhibiting leukocyte influx. This effect, mediated by opioid receptors, involves decreased plasma chemotactic factors and enhanced leukocyte activity.
Area of Science:
- Comparative immunology
- Pharmacology
Background:
- Peritoneal inflammation serves as a model to study drug effects across species.
- Morphine's immunomodulatory role requires further investigation in diverse vertebrates.
Purpose of the Study:
- To compare the anti-inflammatory effects of morphine in phylogenetically distant vertebrates (salmon and mice).
- To elucidate the mechanisms underlying morphine's modulation of peritoneal inflammation.
Main Methods:
- Intraperitoneal injection of morphine and thioglycollate in salmon and mice.
- Quantification of peritoneal leukocytes and assessment of respiratory burst activity.
- Measurement of plasma chemotactic factors and reversal studies with naltrexone.
Main Results:
- Morphine significantly inhibited leukocyte influx into the peritoneal cavity in both species.
- Enhanced leukocyte activity (respiratory burst) was observed in morphine-treated animals.
- Reduced plasma chemotactic factors correlated with inhibited leukocyte migration, reversed by naltrexone.
Conclusions:
- Morphine exerts anti-inflammatory effects by reducing leukocyte numbers and potentially altering their migration via opioid receptors.
- The findings highlight conserved mechanisms of opioid receptor-mediated immunomodulation across vertebrate species.
- Naltrexone pretreatment reversed morphine's effects, confirming the involvement of opioid receptors.