2013 Fiscal Year Final Research Report
The internalization mechanism of Ureaplasma parvum in HeLa cells.
| Project/Area Number |
23791241
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Research Institute, Osaka Medical Center for Maternal and Child Health |
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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), その他部局等, 流動研究員 (60599596)
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| Project Period (FY) |
2011 – 2013
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| Keywords | ウレアプラズマ / 絨毛膜羊膜炎 / エンドサイトーシス |
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| Research Abstract |
Ureaplasma parvum (U. parvum) is a causative of preterm delivery and colonizes human urogenital tract. In order to clarify the intracellular viability of U. paravum in the host cells, U. parvum was challenged to HeLa cells. U. parvum accumulated in the perinuclear region of the HeLa cells within 48 h after infection. Internalization of U. parvum into the HeLa cells was suppressed both by the clathrin-dependent endocytosis inhibitor chlorpromazine hydrochloride (CPZ) and the siRNA. These experiments indicated that U. parvum was internalized into HeLa cells via clathrin-mediated endocytosis. U. parvum were colocalized with early to late endosome markers. The increased production of ROS was observed in the U. parvum infected cells, which lead to structural changes in the mitochondrial cristae and swelling of mitochondria. Our findings raise the possibility that CPZ may have a potential role in the phylaxis of U. parvum infections.
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[Journal Article] S1-1/RBM10 : Multiplicity and cooperativity of nuclear localization domains2013
Author(s)
Xiao S. J., Wang L. Y., Kimura, M., Kojima H., Kunimoto H., Nishiumi F., Yamamoto N., Nishio K., Fujimoto S., Kato T., Kitagawa S., Yamane H., Nakajima K., Inoue A.
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Journal Title
Biol. Cell
Volume: 105(4)
Pages: 162-174
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