Allergy sufferers know too well the itchy, sneezing effects of the release of histamine. This neurotransmitter, produced primarily by white blood cells such as mast cells, eosinophils and basophils, can be suppressed with chemical antihistamines. Indeed, while histamine is involved in some 23 physiological functions including gastric acid release its most studied role is in the inflammatory response during an allergic reaction.
Histamine is derived from the amino acid histidine catalyzed by the enzyme l-histidine decarboxylase. Histamine is stored or broken down by the enzymes histamine-N-methyltransferase or diamine oxidase (DAO). Metabolites from these processes are further degraded by the enzymes monoamine oxidase and aldehyde dehydrogenase.
Histamine and other chemicals are released from mast cells when patrolling IgE antibodies detect an allergen. Histamine, in turn, signals to receptors on tissue cells to increase vascular permeability, leaking fluid at the skin and mucous membranes. The resulting inflammation manifests as itchy hives or wheals, sneezing, watery eyes. Histamine also causes vasodilation and a drop in blood pressure.
Histamine-rich foods and beverages include alcohol, fermented foods, dairy. For those unable to inactivate histamine effectively, it can accumulate and lead to reactivity.
Histamine was isolated in 1927 by British pharmacologist Henry Dale (1875–1968) who found that adrenolytic benzodioxan could block the neurotransmitter in animal models. American chemist George Rieveschl (1916– 2007) created a compound called diphenhydramine that also blocked histamine by binding to H1 receptor sites. Diphenhydramine was renamed Benadryl after Rieveschl patented and licensed the product in 1946.
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