Most food allergies are caused by immunoglobulin epsilon (IgE)-dependent immediate immune responses.　Upon ingestion of allergens that act as antigens, antigen-specific IgE antibodies are produced in the body, and sensitization is established through the binding of IgE antibodies to highaffinity IgE receptors on mast ells.　When the same allergen invades again, owing to the acquired immune sensitivity, it binds to the specific IgE antibodies, thereby degranulating histamine and serotonin.　Histamine is one of the several compounds responsible for causing allergic symptoms, and is synthesized via histidine decarboxylation by histidine decarboxylase (HDC).　As it is one of the essential amino acids, the body obtains this compound through its diet.　In this study, the influence of high levels of histidine on the synthesis and the degranulation of histamine were examined.
L-histidine and a dipeptide of L-histidine, L-carnosine, were added to RBL-2H3 cells (rat basophil leukemia model) at a final concentration of 0.5 mM or 1 mM and incubated for 3 hours.　After incubation, degranulation was induced via antigen-antibody reaction using IgE antibodies in combination with antigens or A23187, a calcium ionophore.　The b-hexosaminidase release rate (%), a degranulation index, was calculated.　Expression of the HDC gene was also detected using the reverse transcription polymerase chain reaction (RT-PCR) technique.
The results indicate that the induction of degranulation was promoted by the addition of Lhistidine, particularly by L-carnosine.　However, the expression of the HDC gene was reduced due to the addition of L-histidine or L-carnosine.　Thus, induction of degranulation was found to be promoted when histidine or carnosine levels were high, indicating the possibility that L-histidine and Lcarnosine
are potential causes of allergic symptoms.　However, the mechanisms involved in the
stimulation of histamine synthesis and induction of degranulation that subsequently reduced HDC gene expression remain unclear.　Hence, further research is needed to clarify these stimulatory mechanisms and explore the potential for preventing the onset and exacerbation of allergic symptoms by adjusting the quantity of histidine obtained through the diet