Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology
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J Neuroimmune Pharmacol · Mar 2010
ReviewNon-CB1, non-CB2 receptors for endocannabinoids, plant cannabinoids, and synthetic cannabimimetics: focus on G-protein-coupled receptors and transient receptor potential channels.
The molecular mechanism of action of Delta(9)-tetrahydrocannabinol (THC), the psychotropic constituent of Cannabis, has been a puzzle during the three decades separating its characterization, in 1964, and the cloning, in the 1990s, of cannabinoid CB1 and CB2 receptors. However, while these latter proteins do mediate most of the pharmacological actions of THC, they do not seem to act as receptors for other plant cannabinoids (phytocannabinoids), nor are they the unique targets of the endogenous lipids that were originally identified in animals as agonists of CB1 and CB2 receptors, and named endocannabinoids. ⋯ In particular, the endocannabinoid anandamide, and the other most abundant Cannabis constituent, cannabidiol, seem to be the most "promiscuous" of these compounds. In this article, we review the latest data on the non-CB1, non-CB2 receptors suggested so far for endocannabinoids and plant or synthetic cannabinoids, and lay special emphasis on uncharacterized or orphan G-protein-coupled receptors as well as on transient receptor potential channels.
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J Neuroimmune Pharmacol · Dec 2008
ReviewOpioids and infections in the intensive care unit should clinicians and patients be concerned?
There is a large body of experimental evidence in research animals and in vitro models that opioids suppress the immune system. If this effect occurs in acute human disease, then patients cared for in Intensive Care Units (ICUs) would be a particularly vulnerable population. ⋯ We review the epidemiology of ICU infections and the pharmacoepidemiology of opioid use in critically ill patients. We critique the limited human research examining the relationship between opioids and infection and make recommendations on designing future clinical studies that could close the knowledge gap about the true hazards of opioid use in hospitalized patients.
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J Neuroimmune Pharmacol · Dec 2007
ReviewThe protective effect of ischemic postconditioning against ischemic injury: from the heart to the brain.
Postconditioning, a series of mechanical interruptions of reperfusion after ischemia, prevents ischemia/reperfusion injury in myocardial infarction. The extensive studies of postconditioning in myocardial infarction have led to clinical trials. This article reviews the protective effects of postconditioning against ischemia from the heart to the brain and provides insights on how studies of postconditioning in the field of heart ischemia have shed light on postconditioning of the brain. ⋯ Future studies should further identify parameters that generate the strongest protection for postconditioning against cerebral ischemia and should study whether postconditioning provides long-term protection. In addition, clarification of the underlying protective mechanisms should be pursued. This will certainly enhance our understanding of this novel phenomenon and may provide important clues for developing pharmacological analogues for stroke treatment.
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J Neuroimmune Pharmacol · Dec 2006
ReviewA role for corticosterone in impaired intestinal immunity and barrier function in a rodent model of acute alcohol intoxication and burn injury.
Alcohol (EtOH) intoxication and burn injury independently activate hypothalamic-pituitary-adrenal (HPA) axis, and glucocorticoids, the end product of the HPA axis, play a role in shaping the immune response under those conditions. By utilizing a rat model of acute EtOH intoxication and burn injury, studies in our laboratory have investigated the role of corticosterone (i.e., glucocorticoids in rodents) in altered intestinal immunity and barrier function following a combined insult of EtOH and burn injury. ⋯ Furthermore, we found that corticosterone does not directly alter the intestinal barrier function; rather, it up-regulates interleukin-18, which then directly or indirectly contributes to impaired intestinal barrier function. The loss of intestinal immunity/barrier function may result in increased bacterial translocation and thereby contribute to postinjury pathogenesis, leading to sepsis and organ dysfunction in burn patients as well as in patients with a history of EtOH intoxication.