Intracellular fate of <i>Ureaplasma parvum</i> entrapped by host cellular autophagy

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  • Fumiko Nishiumi
    Department of Developmental Medicine Osaka Medical Center and Research Institute for Maternal and Child Health Osaka Japan
  • Michinaga Ogawa
    Department of Bacteriology I National Institute of Infectious Diseases Tokyo Japan
  • Yukiko Nakura
    Department of Developmental Medicine Osaka Medical Center and Research Institute for Maternal and Child Health Osaka Japan
  • Yusuke Hamada
    Department of Pediatrics Osaka University Graduate School of Medicine Osaka Japan
  • Masahiro Nakayama
    Department of Pathology Osaka Medical Center and Research Institute for Maternal and Child Health Osaka Japan
  • Jiro Mitobe
    Department of Bacteriology I National Institute of Infectious Diseases Tokyo Japan
  • Atsushi Hiraide
    Critical Care Medical Center Faculty of Medicine Kindai University Osaka Japan
  • Norio Sakai
    Department of Pediatrics Osaka University Graduate School of Medicine Osaka Japan
  • Makoto Takeuchi
    Department of Pathology Osaka Medical Center and Research Institute for Maternal and Child Health Osaka Japan
  • Tamotsu Yoshimori
    Department of Genetics Graduate School of Medicine Osaka University Osaka Japan
  • Itaru Yanagihara
    Department of Developmental Medicine Osaka Medical Center and Research Institute for Maternal and Child Health Osaka Japan

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<jats:title>Abstract</jats:title><jats:p>Genital mycoplasmas, including <jats:italic>Ureaplasma</jats:italic> spp., are among the smallest human pathogenic bacteria and are associated with preterm birth. Electron microscopic observation of <jats:italic>U. parvum</jats:italic> showed that these prokaryotes have a regular, spherical shape with a mean diameter of 146 nm. <jats:italic>U. parvum</jats:italic> was internalized into HeLa cells by clathrin‐mediated endocytosis and survived for at least 14 days around the perinuclear region. Intracellular <jats:italic>U. parvum</jats:italic> reached endosomes in HeLa cells labeled with <jats:styled-content style="fixed-case">EEA</jats:styled-content>1, Rab7, and <jats:styled-content style="fixed-case">LAMP</jats:styled-content>‐1 within 1 to 3 hr. After 3 hr of infection, <jats:italic>U. parvum</jats:italic> induced the cytosolic accumulation of galectin‐3 and was subsequently entrapped by the autophagy marker <jats:styled-content style="fixed-case">LC</jats:styled-content>3. However, when using <jats:italic>atg7</jats:italic><jats:sup>−/−</jats:sup> <jats:styled-content style="fixed-case">MEF</jats:styled-content> cells, autophagy was inadequate for the complete elimination of <jats:italic>U. parvum</jats:italic> in HeLa cells<jats:italic>. U. parvum</jats:italic> also colocalized with the recycling endosome marker Rab11. Furthermore, the exosomes purified from infected HeLa cell culture medium included <jats:italic>U. parvum</jats:italic>. In these purified exosomes ureaplasma lipoprotein multiple banded antigen, host cellular annexin A2, <jats:styled-content style="fixed-case">CD</jats:styled-content>9, and <jats:styled-content style="fixed-case">CD</jats:styled-content>63 were detected. This research has successfully shown that <jats:italic>Ureaplasma</jats:italic> spp. utilize the host cellular membrane compartments possibly to evade the host immune system.</jats:p>

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