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Mast cells are distributed throughout the body and without any doubt are a major cellular source of histamine in the organism. Decarboxylation of histidine to form histamine takes place in Golgi apparatus and then this amine is stored in cytoplasmic secretory granules as a complex with proteoglycans at acidic pH. Histamine is released together with other preformed mediators during mast cell degranulation and it dissociates in tissues from the proteoglycan-histamine complex by cation exchange with extracellular sodium and at neutral pH. It is well known that cross-linking of high affinity IgE receptors (FcεRI) stimulates mast cell degranulation and histamine release. However, there is emerging evidence that receptors for IgG (FcνR) can also activate mast cells to histamine release. Moreover, it is now well established that several endogenous factors, such as some proinflammatory molecules, defensins, cathelicidins, neuropeptides, different cytokines and chemokines, as well as other cell-derived peptides induce histamine release from mast cells. Mast cells also degranulate in response to some bacterial cell wall components and bacterial toxins. Nowadays, it is documented that mast cells express specific histamine receptors, such as H1, H2 and H4, thus it can be presumed that histamine, together with other humoral factors might affect tissue mast cells homeostasis and reactivity, and might regulate its own secretion, as well. [ABSTRACT FROM AUTHOR]