Anti‑allergic action of bacillus Calmette‑Guerin extract in experimental mast cell‑mediated anaphylactic models.

Allergy is an acquired hypersensitivity reaction of the immune system mediated by IgE‑induced mast cell degranulation. In China, bacillus Calmette‑Guerin extract (BCGE) has been shown to be clinically effective for regulating immunity, which enhances the resistance of the body to anaphylactic disease, infectious diseases and cancer. However, the mechanisms remain to be fully elucidated. The present study investigated the potential anti‑allergic effects of BCGE in animal models of mast cell‑dependent anaphylaxis and mechanisms of BCGE in mast cells. Anti‑allergic actions of BCGE were evaluated in passive cutaneous anaphylaxis, dextran T40‑induced scratching behavior mouse models, and in ovalbumin (OVA)‑induced contraction of intestinal tube isolated from OVA‑sensitized guinea pigs. Direct mast cell‑stabilizing effects of BCGE were examined in mast cells from the abdominal cavity of OVA‑sensitized rats. Anti‑allergic signaling mechanisms of BCGE in mast cells were investigated by detection of cyclic adenosine monophosphate levels and protein kinase A expression in mast cells. It was observed that BCGE prevented OVA‑induced cutaneous vascular hyperpermeability, skin itching, elevation in plasma histamine levels and abdominal cavity fluid mast cell degranulation in animal models, in a dose‑dependent manner. BCGE also suppressed OVA‑mediated guinea pig intestinal tube contraction in vitro. In addition, BCGE was found to increase the levels of interferon‑γ, and reduce the levels of interleukin‑4 and OVA‑sIg E levels in OVA‑sensitized rats. BCGE also increased levels of cyclic adenosine monophosphate and the expression of protein kinase A in mast cells separated from the abdominal cavity fluid of OVA‑sensitized rats. In conclusion, the results suggested that BCGE possesses anti‑allergic activity by inhibiting IgE‑induced mast cell degranulation, providing a foundation for the development of BCGE for the treatment of mast cell‑mediated allergic disorders. [ABSTRACT FROM AUTHOR]