Effect of bacterial signal molecule AI-2 on the metabolism and pathogenicity of protozoa

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19113
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Parasitology (including sanitary zoology)
• Research Institution: Hokkaido University
• Principal Investigator: Okubo Torahiko 北海道大学, 保健科学研究院, 講師 (90762196)
• Co-Investigator(Renkei-kenkyūsha): YAMAGUCHI Hiroyuki 北海道大学, 大学院保健科学研究院, 教授 (40221650) ; MATSUO Junji 北海道大学, 大学院保健科学研究院, 講師 (50359486) ; NAKAMURA Shinji 順天堂大学, 医学研究科, 助教 (40207882)
• Research Collaborator: MATSUSHITA Mizue ; AKIZAWA Kouji ; HAYASAKA Kasumi ; FUKUMOTO Tatsuya ; IWASAKI Sumio
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 微生物間相互作用 / 薬剤耐性菌 / 原生生物

Outline of Final Research Achievements

AI-2 is a bacterial signal molecule which is used for bacterial closs talk. In our previous studies, we reported that co-cultivation of bacteria and protozoa causes the raise of AI-2 concentration in the solution. However, the effect of AI-2 on protozoa was not reported. In this study, we compared phenotypic characteristics of protozoa under the presence or absence of AI-2. Our results showed that AI-2 causes the raise of mobility of amoeba cells in a concentraion dependent manner on solid agar surfaces. This suggests that amoeba can detect AI-2 concentration and control its mobility. We showed cross-Kingdom effect of AI-2 on protozoa for the first time.

Free Research Field

細菌学