177 research outputs found
Anti-allergic Drugs
No full textALLERGY is defined as a disease following a response by the IMMUNE SYSTEM to an otherwise innocuous antigen. Allergic diseases include allergic rhinitis, atopic dermatitis, systemic ANAPHYLAXIS, food ALLERGY, allergic ASTHMA and acute urticaria and are mediated by unwanted type-I HYPERSENSITIVITY reactions (see Chap. A9) to extrinsic ALLERGENS like pollen, house dust, animal dander, drugs and insect venom. These diseases are characterised by the production of IgE ANTIBODIES to the allergen that binds to the high-AFFINITY IgE RECEPTOR, FcεRI, on mast cells and BASOPHILS. Binding of allergen to IgE cross-links these RECEPTORS and causes the release of chemical mediators from MAST CELLS, leading to the development of a type-I HYPERSENSITIVITY reaction (Fig. 22.1). This acute response is often followed by a late and more sustained inflammatory response characterised by the recruitment of other EFFECTOR CELLS such as EOSINOPHILS and T helper type-2 (Th2) LYMPHOCYTES. Among the mainstays in the drug treatment of allergic INFLAMMATION, glucocorticosteroids remain the most potent inhibitors, and the reader is referred to Chap. C13 for detailed discussion of these drugs. The use of SPECIFIC IMMUNOTHERAPY in severe allergies is considered in Chap. C5. This present chapter focuses on anti-allergic drugs that specifically TARGET the activation of the mast cell or block the effects of its chemical mediators, in particular HISTAMINE.</p
Pro-inflammatory activity in rats of thiocyanate, a metabolite of the hydrocyanic acid inhaled from tobacco smoke
No full textMichael Wellesley Whitehouse and Mark Jone
Pharmacoepigenetics of the role of DNA methylation in μ-opioid receptor expression in different human brain regions
No full textAim: Exposure to opioids has been associated with epigenetic effects. Studies in rodents suggested a role of varying degrees of DNA methylation in the differential regulation of μ-opioid receptor expression across the brain.
Methods: In a translational investigation, using tissue acquired postmortem from 21 brain regions of former opiate addicts, representing a human cohort with chronic opioid exposure, μ-opioid receptor expression was analyzed at the level of DNA methylation, mRNA and protein.
Results & conclusion: While high or low μ-opioid receptor expression significantly correlated with local OPRM1 mRNA levels, there was no corresponding association with OPRM1 methylation status. Additional experiments in human cell lines showed that changes in DNA methylation associated with changes in μ-opioid expression were an order of magnitude greater than differences in brain. Hence, different degrees of DNA methylation associated with chronic opioid exposure are unlikely to exert a major role in the region-specificity of μ-opioid receptor expression in the human brain
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