| 1. |
Shuge Gui, Zhou Wu, Tomomi Sato, Takashi Kanematsu, LPS from P. gingivalis enhances inflammatory responses of microglia during exposure to amyloid ｂ
, 第97回日本薬理学会年会, 2023.12, 【Background】 Brain amyloid beta is accumulated from 20 years before Alzheimer's disease (AD) onset, and microglia is implicated in promoting AD pathogenesis. LPS from P. gingivalis (PgLPS), the periodontal bacteria, is detected in AD brain. 【Aim】 In this study, we test our hypothesis that PgLPS enhances microglia-mediated neuroinflammtion in amyloid beta exposure environment.【Methods & Results】 MG6 microglial cells were exposed to PgLPS (0.1 micro g/mL), amyloid beta (0.1micro M) or co-exposed to amyloid beta and PgLPS. Inflammatory mediators and NFkB signaling were examined. In comparison to control MG6 cells, mRNA expressions of TNF-α, IL-1beta and IL-6 were induced from 1 h after exposure to PgLPS but not amyloid beta. Interestingly, mRNA expressions of TNF-α, IL-1beta and IL-6 were significantly increased in amyloid beta and PgLPS co-exposed (AL) MG6 cells from 3 h in compassion to those in PgLPS-exposed cells. TNF-α production were significantly elevated in AL-exposed MG6 cells from 3 h in compassion to that in PgLPS-exposed ones. Furthermore, phosphorylation of IκB and nuclear translocation of p65 NF-κB were up-regulated in PgLPS-exposed MG6 cells but not that in amyloid beta-exposed cells. Phosphorylation of IκB and nuclear translocation of p65 NF-κB were significantly up-regulated in AL-exposed MG6 cells in compassion to that in PgLPS-exposed cells. 【Conclusion】 The observations strongly suggest that PgLPS enhances microglia-related neuroinflammtion in amyloid beta exposure environment. The present study provides a new mechanism of periodontitis involving in the early pathologies of AD. . |
| 2. |
Yebo Gu, Junjun Ni, Zhou Wu, Ichiro Takahashi, Chronic systemic exposure of Lipopolysaccharide from Porphyromonas gingivalis induces memory decline through the upregulation of the bone loss promotion molecule IL-17 in middle-aged mice, 第72回日本薬理学会西南部会, 2019.11. |
| 3. |
Yebo Gu, Junjun Ni, Zhou Wu, Ichiro Takahashi, Chronic systemic exposure of PgLPS induces long bone loss and cognitive decline in middle-aged mice, 第78回日本矯正歯科学会, 2019.11. |
| 4. |
Junjun Ni, Hiroshi Nakanishi and Zhou Wu , An impaired intrinsic microglial clock system induces neuroinflammatory alterations in the early stage of amyloid precursor protein knock-in mouse brain
, 第72回日本薬理学会西南部会, 2019.11. |
| 5. |
Yebo Gu, Junjun Ni, Muzhou Jiang, Zhou Wu, Ichiro Takahashi, Chronic systemic exposure of Lipopolysaccharide from Porphyromonas gingivalis
induces Memory decline and Bone loss in Middle-aged Mice, 6th Congress of ASCNP, 2019.10. |
| 6. |
Fan Zeng, Junjun Ni, Zhou Wu , Porphyromonas gingivalis infection increases RAGE production in
hCMEC/D3 cell line, 6th Congress of ASCNP, 2019.10. |
| 7. |
Wanyi Huang, Junjun Ni, Zhou Wu,, Porphyromonas gingivalis infected Leptomeningeal Cells Reduces Synapses Proteins in Primary Cultured Neurons, 6th Congress of AsCNP, 2019.10. |
| 8. |
Muzhou Jiang, Junjun Ni, Yebo Gu, Zhou Wu, Microglia induces tau hyperphosphorylation of cultured neurons after exposure to Porphyromonas gingivalis LPS, 6th Congress of ASCNP, 2019.10. |
| 9. |
Zhou WU, Inflammation and Lysosomal Enzymes: Prevention Approach of Cognitive Decline, Neurology Conference , 2019.06. |
| 10. |
武 洲, Mechanism of Cathepsins involving Alzheimer’s disease: Linking systemic inflammation & neuroinflammation, 北理工大学教育セミナー, 2017.11. |
| 11. |
Wu Z, Cathepsin B, novel therapeutic target for microglia-mediated neuroinflammation, special seminar in University of Southampton, 2017.02. |
| 12. |
Hiro Take, Oral health and healthy life expectancy, The 1st International Symposium for Women Researchers on Advanced Science and Technology conjugated with Seminar for Young Researchers, 2016.07. |
| 13. |
Yicong Liu, 武 洲, 中西 博, 歯周病とアルツハイマー病（AD）（1）： Porphyromonas gingivalis由来LPSによるマクロファージ活性化と脳髄膜を介した末梢炎症シグナルの脳内伝播とミクログリア活性化, 第57回歯科基礎医学会, 2015.09. |
| 14. |
武 洲, NI JUNJUN, 中西 博, 歯周病とアルツハイマー病（AD）（2）：Porphyromonas gingivalis由来LPSの慢性的末梢投与によって誘発されるAD様フェノタイプにおけるカテプシンBの役割, 第57回歯科基礎医学会, 2015.09. |
| 15. |
Hiro Take, Ryo Okada, NI JUNJUN, Hiroshi Nakanishi, Involvement of brain pericyte damage in neuropathological
changes associated with lysosomal storage, International Conference on Neurology & Therapeutics, 2015.07. |
| 16. |
Hiro Take, Oral health, Nutrition and healthy life expectancy, 9th CASPN, 2015.05. |
| 17. |
Hiro Take, The Profound Impact of Oral health on Aging Societ, 吉林大学歯学部創立30周年 学術大会, 2015.05. |
| 18. |
武 洲, 中西 博, 歯周病によるアルツハイマー様病態の促進メカニズム, 第87回日本薬理年会, 2015.03. |
| 19. |
Hiro Take, Porphyromonas gingivalis LPS induces microglial activation and A beta accumulation in the brain DepartmentCathepsin B-dependent novel IL-1beta production pathway in microglia,, Kudai Oral Bioscience 2014, 2014.03. |
| 20. |
Hiro Take, Hiroshi Nakanishi, Potential roles of chromogranin A in cathepsin B-dependent IL-1bata production by microglia in Alzheimer’s disease,, 第86回日本薬理学会年会, 2013.03. |
| 21. |
Hiro Take, Gatekeeper of chronic inflammation: Cathepsin B-dependent Novel IL-1beta Production Pathway, School of Stomalogy, Jilin University, Changchun, China,, 2013.03. |
| 22. |
Hiro Take, Gatekeeper of chronic inflammation: Cathepsin B-dependent Novel IL-1beta Production Pathway, School of Stomalogy, Jilin University, Changchun, China,, 2013.03. |
| 23. |
Hiro Take, Hiroshi Nakanishi, Cathepsin B-dependent Novel IL-1β Production Pathway in Microglia, Kyudai Oral Bioscience 2013, 2012.03. |
| 24. |
Wu Z, Nakanishi H., Age-dependent differentiatial regulation of tight junction proteins in the leptomeninges by glial cells during systemic inflammation., Neuroscience 2008, 2008.11. |
| 25. |
Phosphatidylserine-containing liposomes inhibit the differentiation of osteoclasts and trabecular bone loss. |
| 26. |
Zhou Wu, Yukie Tokuda, Xin-Wen Zhang, and Hiroshi Nakanishi, Age-dependent differential modulation of the barrier function of the leptomeninges in the cerebral cortex by activated glial cells during the systemic inflammation, XXVI CINP CONGRESS , 2008.07. |
