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Histamine has been recognized as a major mediator in allergic diseases such as allergic rhinitis, chronic rhinosinusitis, and nasal polyps. Histamine gets released by lymphocytes, neutrophils, platelets, macrophages, and eosinophils, also endothelial cells and nasal lavage fluid produces histamine released factors. This heterogeneous group of factors causing basophil degranulation may also recruit mast cell or basophil participation in late-phase allergic reactions and other chronic inflammatory conditions. Histamine H1 receptor (H1R), originally derived from bovine, is known to be expressed in many human tissues including airway, intestinal and vascular smooth muscle and brain. Histamine-1 receptor (H1R) antagonists control clinical symptoms related to histamine expression and H1R is a primary receptor of histamine activity. Immunohistochemical studies have shown that strong immune responses to H1R in vascular endothelial cells increase vascular permeability, leukocyte infiltration, and edema formation. Nevertheless, the mechanism of this effect has not been clearly understood.

Histamine Induced Production of Chemokine CXCL8 Through H1R/PLC and NF-κB Signaling Pathways in Nasal Fibroblasts