The elucidation of the mechanisms behind the allergic reaction induced by tryptophan supplement byproducts.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460804
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Hygiene and public health
• Research Institution: Ehime University
• Principal Investigator: OKAMOTO Takeaki 愛媛大学, 教育学部, 准教授 (20398431)
• Co-Investigator(Kenkyū-buntansha): SUGAHARA Takuya 愛媛大学, 農学部, 教授 (00263963)
• Co-Investigator(Renkei-kenkyūsha): YAMAUCHI Akira 川崎医科大学, 医学部, 准教授 (80372431) ; KATO Tadahiro 愛媛大学, 教育学部, 准教授 (60325363)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: トリプトファン / 好酸球 / 不純物 / 好中球 / 走化性 / ケモカインレセプター / ケモカイン

Outline of Final Research Achievements

The expression of CXCR1 and CXCR2, and the eotaxin receptor, CCR3, in human eosinophils exposed to the contaminant 3-phenylamino-L-alanine (PAA). Chemotactic activity and CXCR1 and CXCR2 expression increased after PAA exposure in a dose-dependent manner. The CXCR2 expression level was higher than that of CXCR1. These data suggest a strong correlation between chemotactic activity and IL-8 receptor expression in eosinophils exposed to PAA. In contrast, the expression of CCR3 was inhibited by PAA in a dose-dependent manner. These results suggest that the eosinophils partially lost their original character and partially adopted the character of neutrophils upon exposure to PAA. Therefore, we suggest an eosinophilia-myalgia syndrome (EMS) onset mechanism, based on the findings that PAA increased the expression of IL-8 receptors in human eosinophils, which then developed chemotaxis to IL-8, an inflammatory chemokine, leading to further inflammation that may result in EMS onset.

Free Research Field

食品免疫学、食品衛生学