Analysis of U. parvum infection mechanism

2016 Fiscal Year Final Research Report

• Project/Area Number: 26860859
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Embryonic/Neonatal medicine
• Research Institution: Research Institute, Osaka Medical Center for Maternal and Child Health
• Principal Investigator: Nishiumi Fumiko 地方独立行政法人大阪府立病院機構大阪府立母子保健総合医療センター(研究所), 免疫部門, 流動研究員 (60599596)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: ウレアプラズマ / 絨毛膜羊膜炎 / オートファジー / エクソサイトーシス

Outline of Final Research Achievements

Genital mycoplasmas, including Ureaplasma spp., are among the smallest human pathogenic bacteria and are associated with preterm birth. U. parvum was internalized into HeLa cells by clathrin-mediated endocytosis and survived for at least 14 days around the perinuclear region. After 3 h of infection, U. parvum induced the cytosolic accumulation of galectin-3 and was subsequently entrapped by the autophagy marker LC3. However, when using atg7－/－ MEF cells, autophagy was inadequate for the complete elimination of U. parvum in HeLa cells. U. parvum also colocalized with the recycling endosome marker Rab11. Furthermore, the exosomes purified from infected HeLa cell culture medium included U. parvum. In these purified exosomes ureaplasma lipoprotein multiple banded antigen, host cellular annexin A2, CD9, and CD63 were detected. This research has successfully shown that Ureaplasma spp. utilize the host cellular membrane compartments possibly to evade the host immune system.

Free Research Field

医歯薬学