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Opioids immune interactions

Considerable evidence for opioid-chemokine interactions comes from studies of pain and inflammation, where the inherent relationships between pain, inflammation, and the counteracting antinociceptive influences of opioids have considerable biomedical implications. The adaptive changes in immune and nervous system function with chronic inflammation and pain further reveal the inherent interrelatedness between opioids (Ossipov et al. 2003 Evans 2004 Roy et al. 2006 Christie 2008)... [Pg.354]

Interaction Between Opioid and Chemokine Receptors in Immune Cells Implications for HIV Infection... [Pg.319]

Suzuki S, Chuang LE, Yau P, Doi RH, Chuang RY (2002b) Interactions of opioid and chemokine receptors oligomerization of mu, kappa, and delta with CCR5 on immune cells. Exp Cell Res 280 192-200... [Pg.336]

Stevia Stevia rebaudiana) Uses Natural sweetener, hypoglycemic and hypotensive properties Actions Multiple chemical components sweetness d/t glycoside, stevioside hypotensive effect may be d/t diuretic action or vasodilation action Available forms Liq extract, powder, caps Notes/SE HA, dizziness, bloating Interactions T Hypotensive effects W/ antihypertensives esp CCB, diuretics EMS Monitor BP does not encourage dental caries may -1-glucose St. John s Wort (Hypericum perforatum) Uses Mild-mod depression, anxiety, anti-inflammatory, immune stimulant/anti-HIV/antiviral, gastritis, insomnia, vitiligo Action MAOI in vitro, not in vivo bacteriostatic bactericidal, T capillary blood flow, uterotonic activity in animals Efficacy Variable benefit w/ mild-mod depression in several trials, but not always seen in clinical practice Available forms Teas, tabs, caps, tine, oil ext for topical use Dose 2-4 g of herb or 0.2-1 mg of total hypericin (standardized extract) daily Notes/SE Photosensitivity (use sunscreen) rash, dizziness, dry mouth, GI distress Interactions Enhance MAOI activity, EtOH, narcotics, sympathomimetics EMS T Risk of photosensitivity Rxns t effects of opioids and sympathomimetics... [Pg.334]

The finding that the immune and neuroendocrine systems both express receptors for opioids and for ACTH and that both systems can synthesize and release peptides active at these receptors, led to the suggestion that the immune system functions as a sensory organ (Blalock, 1984, 1999) and that this forms the basis for the interaction betw een the tw o systems. It is v ell knovm that the nervous system responds to a variety of stimuli and, w hen appropriate, releases neurotransmitters and hormones that enable an appropriate reaction to these stimuli or stresses. This can include changes in immune system function. Blalock proposed that the immune system also responds to particular stimuli, in this case environmental changes that would not be readily detec ted by the nervous system, such as the presence of bacteria or viruses. In response, the immune system releases a variety of compounds, including peptide hormones that will alter both immune and nervous system function. [Pg.485]

The function of nociceptin in the immune system and/or in the interaction betw een the nervous and immune systems is not clear at present. Studies suggest that it increases T cell activation, suppresses antibody production and is a potent chemoattractant. However, given the presence of both the neuropeptide and its receptor in immune cells, analogous to beta-endoiphin and the enkephalins, nociceptin is well positioned to play a role similar to that of the better-known and studied opioid-like peptides. [Pg.486]

Knowledge of the interaction of benzodiazepines and the immune system is much less advanced compared to our understanding of interactions between opioid systems and the immune system. It is clear that the benzodiazepines have strong anti-anxiety effects and that through these actions they reduce the response to stressful situations (Zavala, 1997). This, in turn, will reduce stress-induced activation of the HPA axis and so reduce its regulatory effects on the immune system. These effects are centrally mediated, however, and can be considered indirect effects. [Pg.554]

At the molecular level intravenous anaesthetics interact mainly with GABAa receptors (thiopental, propofol...) or with other ligand-gated ion channels (ketamine) synthetic opioids (phentanyl congeners) act in a more specific way as agonists of p-opioid receptors. However, all the anaesthetics, in addition to their action at the level of central nervous system, have also a variety of effects at other levels in particular, a temporary impairment of the immune system involving phagocytes can be induced. [Pg.287]


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Opioids interactions

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