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It has been known for more than one hundred years that an intravenous injection of histamine causes a fall in the blood pressure. [30] The underlying mechanism concerns both vascular hyperpermeability and vasodilation. Histamine binding to endothelial cells causes them to contract, thus increasing vascular leak.
In addition, seasonal allergies are known to cause sinus inflammation, but that isn’t the only area that can become inflamed. ... “Histamine is released in the body and enters the ...
The term inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response—the two components are considered together in discussion of infection, and the word is used to imply a microbial invasive cause for the observed inflammatory ...
The production of leukotrienes is usually accompanied by the production of histamine and prostaglandins, which also act as inflammatory mediators. [ 4 ] One of their roles (specifically, leukotriene D 4 ) is to trigger contractions in the smooth muscles lining the bronchioles; their overproduction is a major cause of inflammation in asthma and ...
[8] Ligation of Fc receptors on the surfaces of immune effector cells can give rise to a number of responses, [9] such as degranulation (e.g., of mast cells, causing histamine liberation and subsequent urticaria), phagocytosis, release of pro-inflammatory cytokines and chemokines, platelet activation [10] resulting in the formation of clots, etc.
The antibodies will cause cells in the body to produce histamine. This histamine will act on different areas of the body (eyes, throat, nose, gastrointestinal tract, skin or lungs) to produce symptoms of an allergic reaction. The allergic response is not limited to a certain amount of exposure.
Histamine is a weak base (a compound able to react with a hydrogen ion to form an acid) that can link with acid groups within the granules of the mast cells. [8] The mechanism of the displacement theory. The crux of this theory lies in the assumption that histamine liberators release histamine by displacing it from cells.
When activated, mast cells rapidly release characteristic granules, rich in histamine and heparin, along with various hormonal mediators and chemokines, or chemotactic cytokines into the environment. Histamine dilates blood vessels, causing the characteristic signs of inflammation, and recruits neutrophils and macrophages. [5]