Mast cells as a source of both preformed and immunologically inducible TNF-alpha/cachectin

Article Abstract:

Tumor necrosis factor-alpha (TNF-alpha), also known as cachectin, is a cytokine involved in many bodily functions such as inflammation, infection, metabolism of fats and proteins, maturation of blood cells, development of blood vessels, and immune resistance to parasites and cancer. TNF-alpha is known to be produced by activated macrophages, a type of immune cell that is present in various tissues. TNF-alpha is also known to be produced by mast cells, which are basophils (a type of blood cell found in tissues that is involved in allergic reactions). Activation of mast cells which is dependent on IgE, an immunoglobulin molecule involved in allergic reactions, causes the release of TNF-alpha. This study shows that the release of TNF-alpha from mast cells may be one of the factors that cause the infiltration of cells involved in the inflammatory response, such as the immune response to parasites, immune reactions in asthma and other allergic diseases, the host response to tumors, the regulation of wound healing, the development of blood vessels, and the maturation of blood cells and immune cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Allergy, Immunoglobulin E

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The two faces of the mast cell

Article Abstract:

Mast cells release tumor necrosis factor-alpha (TNF-alpha) which protects the organism from pathogens but also causes the severe acquired immunity reaction, anaphylaxis. The mast cells facilitate the removal of harmful pathogens in mice and decrease mortality. Death due to bacterial peritonitis is suppressed in mast-cell-deficient mice that are reconstituted with mast cell injections. Antibodies against TNF-alpha remove the protective effect of the mast cells. However, in acquired immunity, the TNF-alpha released by the mast cells produces a potentially lethal anaphylactic reaction.

Causes of, Immunology, Anaphylaxis, Natural immunity

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Mast cells promote homeostasis by limiting endothelin-1-induced toxicity

Article Abstract:

The study demonstrate that Endothelin (ET)(sub A)-dependent mast-cell activation can diminish both ET-1 levels and ET-1-induced pathology in vivo, and also can contribute to optimal survival during acute bacterial peritonitis. ET-1 is a 21-amino acid peptide, derived from vascular endothelial cells, with potent vasoconstrictor activity.

United States, Science & research, Endothelin, Peritonitis, Homeostasis

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