Abstract
Morphine coinjection with zymosan inhibits pain and leukocyte accumulation during peritonitis in several strains of mice, and affects systems of endogenous opioids. Present investigations focus on Met-enkephalin (Met-ENK) in the inflamed peritoneal cavity and brain centers of Swiss mice. Males of Swiss mice were IP injected with zymosan or zymosan supplemented with morphine. At the selected time points the peritoneal leukocytes were counted and the Met-ENK level was measured in exudatory fluid and leukocytes, striatum, hypothalamus, and pituitary gland. The Met-ENK content in peritoneal fluid rised sharply after zymosan injection, which corresponded with its decline in exudatory leukocytes, hypothalamus, and striatum. Morphine coinjection enhanced intraperitoneal accumulation of Met-ENK and its release from exudatory leukocytes, but inhibited its early fluctuations in hypothalamus and striatum. Effects of morphine-modulated inflammation on the Met-ENK system lasted longer than 7 days.
Highlights
IntroductionWe wish to draw attention to another model for investigations of the opioid system participation in the inflammatory processes, namely to experimental peritonitis induced by intraperitoneal (IP) injection of a sterile stimulant, for example, zymosan
The immune system plays an important role in the pain control, especially under inflammatory conditions.As evidenced in series of experiments on adjuvantinduced paw inflammation in the rat, opioid receptors on peripheral sensory nerve terminals in the inflamed tissue are upregulated and activated by opioid peptides derived from immunocytes accumulated in the focus of inflammation resulting in potent analgesia [1, 2].We wish to draw attention to another model for investigations of the opioid system participation in the inflammatory processes, namely to experimental peritonitis induced by intraperitoneal (IP) injection of a sterile stimulant, for example, zymosan
The zymosan-induced peritonitis described here follows a typical pattern of inflammatory reaction with a rapid accumulation of PMNs during the initial 24 hours followed by mononuclear leukocytes dominating in peritoneal cavity on the 7th day (Figure 1)
Summary
We wish to draw attention to another model for investigations of the opioid system participation in the inflammatory processes, namely to experimental peritonitis induced by intraperitoneal (IP) injection of a sterile stimulant, for example, zymosan. The convenience of this model consists in the possibility of a precise quantification of inflammation-related cells and soluble factors in samples of exudatory fluid quantitatively retrieved from the control or inflamed peritoneal cavity [3, 4, 5]. We have shown that the supplementation of a stimulant with exogenous opioid, morphine, affects inflammation in a naltrexone-reversed manner, that is, through the binding of opioid receptors. Morphine co-administration significantly reduces the levels of chemotactic factors and the number of inflammatory leukocytes in several
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