2006 Fiscal Year Final Research Report Summary
Analysis of host defense system against pathogenic oral bacteria in oral epithelial cells by the intracellular PAMPs receptors
| Project/Area Number |
17591904
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Tokyo University (2006)
Osaka University (2005) |
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Principal Investigator |
NAKAGAWA Ichiro Tokyo University, Institute of Medical Science International Research Center for Infectious Diseases, Associate Professor, 医科学研究所, 助教授 (70294113)
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| Project Period (FY) |
2005 – 2006
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| Keywords | Group A Streptococcus / autophagy / recognition receptor / miR-RNAi / knockdown / Nalp |
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| Research Abstract |
Macroautophagy(referred to as autophagy) is a unique form of membrane trafficking in which membrane compartments(autophagosome) engulf both organella and cytosolic macromolecules and deliver them to the lysosomes. Many pathogenic bacteria can invade phagocytic and non-phagocytic cells and colonize them intracellularly, then become disseminated to other cells. The endocytic degradation pathway is thought to be the only prevention against such intracellular pathogens. Autophagy, a fundamental cellular homeostasis pathway that operates with the intracellular degradation/recycling system, causes the turnover of cellular components by delivering portions of the cytoplasm and organelles to lysosomes. Recently, we reported that autophagic degradation is a previously unrecognized effector of host innate immunity. Streptococcus pyogenes(Group A Streptococcus ; GAS) successfully enters human epithelial cells via endocytosis. GAS immediately escapes from the endosomes to the cytoplasm and gains a replicative niche, after which GAS in the cytoplasm is trapped in autophagosome-like compartments and degraded upon fusion with lysosomes. This process indicates that autophagy plays a protective role in infectious diseases. We also found that autophagic degradation was induced against Staphylococcus aureus, while methicillin-resistant S.aureus were resistant to autophagic degradation. We also found some intracellular NLRP were related to the recognition of intracellular bacteria to induce autophagosome formation.
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