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Hiroyuki Tada

Section

Graduate School of Dentistry

Job title

Professor

Degree

D. D. S. (Tohoku University)

researchmap

https://researchmap.jp/read0191522

J-GLOBAL ID

200901039079529046

e-Rad No.

70431632

Research History 11

2025/04 - Present

Division of Oral Microbiology and Immunology, Department of Ecological Dentistry, Tohoku University Graduate School of Dentistry　Professor
2017 - 2025/03

東北大学大学院歯学研究科エコロジー歯学講座口腔分子制御学分野　講師
2013 - 2017

Tohoku University　Graduate School of Dentistry
2012 - 2013

Ohu University　Faculty of Dentistry
2011 - 2012

国立長寿医療研究センター　口腔疾患研究部　リサーチレジデント
2008 - 2011

東北大学病院　歯周病科　医員
2007 - 2008

University of Michigan Medical School　Department of Pathology　Research Fellow
2006 - 2007

Akita University
2004 - 2006

Akita University
2003 - 2004

Tohoku University　Graduate School of Dentistry
1998 - 1999

Tohoku University Hospital, Faculty of Dentistry　Department of Periodontology and Endodontology　Clinical Resident

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Education 2

Tohoku University　Graduate School of Dentistry　Doctoral Course

1999/04 - 2003/03
Ohu University　Faculty of Dentistry

1992/04 - 1998/03

Committee Memberships 3

内毒素・LPS研究会　事務局代表

2023 - Present
日本細菌学会東北支部　地方委員

2014/06 - Present
内毒素・LPS研究会　運営委員

2014/06 - Present

Professional Memberships 9

THE JAPANESE SOCIETY FOR IMMUNOLOGY
内毒素・LPS研究会
TOHOKU UNIVERSITY DENTAL SOCIETY
日本エンドトキシン・自然免疫研究会
JAPANESE ASSOCIATION FOR ORAL BIOLOGY
日本細菌学会
日本歯周病学会
日本歯科保存学会
International Association for Dental Research

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Research Interests 6

抗菌ペプチド
生体バリア破綻
Neutrophil extracellular traps
Periodontopathic bacteria
Chronic allergic inflammation
Innate immunity

Research Areas 3

Life sciences / Oral medicine / Oral Microbiology
Life sciences / Conservative dentistry and endodontics / Periodontology
Life sciences / Immunology /

Awards 10

研究奨励金

2020/10　ホクト生物科学振興財団
日本エンドトキシン・自然免疫研究会奨励賞・最優秀賞

2019/11　日本エンドトキシン・自然免疫研究会
研究奨励金

2017/10　ホクト生物科学振興財団
奨励賞

2013　日本歯科保存学会
日本歯科保存学会デンツプライ賞

2010
医学系研究奨励

2009　武田科学振興財団
内藤記念科学振興財団海外研究留学助成

2006
上原記念生命科学財団リサーチフェローシップ

2006
東北開発記念財団海外派遣援助

2003
IADR/Lion Dental Research Award for Junior Investigators

2003

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Papers 41

Cementocyte-derived extracellular vesicles regulate osteoclastogenesis and osteoblastogenesis Peer-reviewed

Li, J., Sakisaka, Y., Nemoto, E., Maruyama, K., Suzuki, S., Xiong, K., Tada, H., Tenkumo, T., Yamada, S.

Journal of Dental Sciences　4　2236-2246　2024/10

DOI： 10.1016/j.jds.2024.02.025 　
Neutrophil extracellular traps inhibit osteoclastogenesis Peer-reviewed

Numazaki K, Tada H, Nishioka T, Nemoto E, Matsushita K, Mizoguchi I, Sugawara S

Biochemical and Biophysical Research Communications　705　149743　2024/02

DOI： 10.1016/j.bbrc.2024.149743 　
Macrophage migration inhibitory factor-mediated mast cell extracellular traps induce inflammatory responses upon Fusobacterium nucleatum infection Peer-reviewed

Tada H, Nishioka T, Ishiyama R, Song LT, Onoue S, Kawahara K, Nemoto E, Matsushita K, Sugawara S

Biochemical and Biophysical Research Communications　674　90-96　2023/06

DOI： 10.1016/j.bbrc.2023.06.060 　
Hericium erinaceus ethanol extract and ergosterol exert anti-inflammatory activities by neutralizing lipopolysaccharide-induced pro-inflammatory cytokine production in human monocytes Peer-reviewed

Tada H, Kawahara K, Osawa H, Song LT, Numazaki K, Kawai J, Onoue S, Nishioka T, Nemoto E, Matsushita K, Sugawara S

Biochemical and Biophysical Research Communications　636　(2)　1-9　2022/12

DOI： 10.1016/j.bbrc.2022.10.090 　
Reactivation of p53 by RITA Induces Apoptosis in Human Oral Squamous Cell Carcinoma Cells Peer-reviewed

Endo M, Nishioka T, Numazaki K, Hasegawa H, Takahashi T, Sugawara S, Tada H

Anticancer Research　42　(6)　2931-2937　2022/06

DOI： 10.21873/anticanres.15775 　
Extracellular Vesicles Derived From Murine Cementoblasts Possess the Potential to Increase Receptor Activator of Nuclear Factor-κB Ligand-Induced Osteoclastogenesis Peer-reviewed

Sato R, Maruyama K, Nemoto E, Sakisaka Y, Suzuki S, Li J, Numazaki K, Tada H, Yamada S

Frontiers in Physiology　13　825596　2022/02

DOI： 10.3389/fphys.2022.825596 　
Porphyromonas gingivalis Gingipains-Mediated Degradation of Plasminogen Activator Inhibitor-1 Leads to Delayed Wound Healing Responses in Human Endothelial Cells International-journal International-coauthorship Peer-reviewed

Song L, Tada H, Nishioka T, Nemoto E, Imamura T, Potempa J, Li CY, Matsushita K, Sugawara S

Journal of Innate Immunity　1-14　2021/11

DOI： 10.1159/000519737. 　
Nitrogen-Containing Bisphosphonates and Lipopolysaccharide Mutually Augment Inflammation via Adenosine Triphosphate (ATP)-Mediated and Interleukin 1β (IL-1β)-Mediated Production of Neutrophil Extracellular Traps (NETs). International-journal Peer-reviewed

Bando K, Kuroishi T, Tada H, Oizumi T, Tanaka Y, Takahashi T, Mizoguchi I, Sugawara S, Endo Y

Journal of Bone and Mineral Research　36　(9)　1866-1878　2021/09

DOI： 10.1002/jbmr.4384 　

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Among the bisphosphonates (BPs), nitrogen-containing BPs (N-BPs) have much stronger anti-bone-resorptive actions than non-N-BPs. However, N-BPs have various side effects such as acute influenza-like reactions after their initial administration and osteonecrosis of the jawbones after repeated administration. The mechanisms underlying such effects remain unclear. To overcome these problems, it is important to profile the inflammatory nature of N-BPs. Here, we analyzed the inflammatory reactions induced in mouse ear pinnae by the N-BPs alendronate (Ale) and zoledronate (Zol). We found the following: (i) Ale and Zol each induced two phases of inflammation (early weak and late strong ear swelling); (ii) both phases were augmented by lipopolysaccharides (LPSs; cell-surface constituent of gram-negative bacteria, including oral bacteria), but prevented by inhibitors of the phosphate transporters of solute carrier 20/34 (SLC20/SLC34); (iii) macrophages and neutrophils were involved in both phases of Ale+LPS-induced ear-swelling; (iv) Ale increased or tended to increase various cytokines, and LPS augmented these effects, especially that on interleukin 1β (IL-1β); (v) adenosine triphosphate (ATP) was involved in both phases, and Ale alone or Ale+LPS increased ATP in ear pinnae; (vi) the augmented late-phase swelling induced by Ale+LPS depended on both IL-1 and neutrophil extracellular traps (NETs; neutrophil-derived net-like complexes); (vii) neutrophils, together with macrophages and dendritic cells, also functioned as IL-1β-producing cells, and upon stimulation with IL-1β, neutrophils produced NETs; (viii) stimulation of the purinergic 2X7 (P2X7) receptors by ATP induced IL-1β in ear pinnae; (ix) NET formation by Ale+LPS was confirmed in gingiva, too. These results suggest that (i) N-BPs induce both early-phase and late-phase inflammation via ATP-production and P2X7 receptor stimulation; (ii) N-BPs and LPS induce mutually augmenting responses both early and late phases via ATP-mediated IL-1β production by neutrophils, macrophages, and/or dendritic cells; and (iii) NET production by IL-1β-stimulated neutrophils may mediate the late phase, leading to prolonged inflammation. These results are discussed in relation to the side effects seen in patients treated with N-BPs. © 2021 American Society for Bone and Mineral Research (ASBMR).
Effects of Zoledronate on Local and Systemic Production of IL-1β, IL-18, and TNF-α in Mice and Augmentation by Lipopolysaccharide International-journal Peer-reviewed

Funayama H, Tashima I, Okada S, Ogawa T, Yagi H, Tada H, Wakita R, Asada Y, Endo Y

Biological and Pharmaceutical Bulletin　42　(6)　929-936　2019/06/01
Publisher: Pharmaceutical Society of Japan
DOI： 10.1248/bpb.b18-00923 　

ISSN： 0918-6158

eISSN： 1347-5215

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Bisphosphonates (BPs) containing nitrogen (N-BPs) exhibit far stronger anti-bone-resorptive effects than non-N-BPs. However, repeated administration of N-BPs causes osteonecrosis selectively in jawbones. As BPs accumulate in large amounts within inflamed bones, any N-BP released from the pool accumulated within jawbones might directly act on cells in the surrounding soft-tissues and induce inflammation or necrosis. Here, we examined the local and systemic effects of zoledronate (the most potent N-BP with the highest incidence of jawbone-necrosis) on inflammatory cytokines in mice. Locally within ear-pinnas: (i) zoledronate induced long-lasting accumulation of interleuikin-1β (IL-1β) and IL-18, but not tumor necrosis factor-α (TNF-α), (ii) zoledronate and lipopolysaccharide (LPS, a cell-wall component of Gram-negative bacteria) mutually augmented the productions of IL-1β, IL-18, and TNF-α, and (iii) oxidronate (a toxic non-N-BP) by itself produced not only IL-1β and IL-18, but also TNF-α. In systemic experiments using intraperitoneal injection of zoledronate and/or LPS, (i) zoledronate by itself increased none of the above cytokines in serum, and (ii) in mice pretreated (3 d before) with zoledronate, the LPS-induced increases in serum IL-1β and IL-18 were greatly augmented with a delayed slight TNF-α augmentation. These results, together with previous ones, suggest that (a) pro-IL-1β and pro-IL-18 accumulate within cells in soft-tissues exposed to N-BPs, and infection may augment not only their production, but also the release of their mature forms, (b) IL-1β and IL-18 (possibly together with TNF-α) may play important roles in N-BP-induced inflammation and/or necrosis, and (c) mechanisms underlying the cytotoxic effects of BPs may differ between N-BPs and non-N-BPs.
Dectin-2-Mediated Signaling Leads to Delayed Skin Wound Healing through Enhanced Neutrophilic Inflammatory Response and Neutrophil Extracellular Traps Formation. International-journal Peer-reviewed

Miura T, Kawakami K, Kanno E, Tanno H, Tada H, Sato N, Masaki A, Yokoyama R, Kawamura K, Kitai Y, Takagi N, Yamaguchi K, Yamaguchi N, Kyo Y, Ishii K, Imai Y, Saijo S, Iwakura Y, Tachi M

Journal of Investigative Dermatology　139　(3)　702-711　2019/03
Publisher: Elsevier BV
DOI： 10.1016/j.jid.2018.10.015 　

ISSN： 0022-202X

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Dendritic cell-associated C-type lectin-2 (i.e., dectin-2) recognizes fungal polysaccharides, including α-mannan. Dectin-2-mediated recognition of fungi, such as Candida albicans, leads to NF-κB activation, which induces production of inflammatory cytokines. However, the role of dectin-2 in skin wound healing remains unclear. In this study, we sought to determine how dectin-2 deficiency and the administration of α-mannan affected the wound healing process. Full-thickness wounds were created on the backs of wild type C57BL/6 and dectin-2-deficient mice. We analyzed wound closure, histological findings, and re-epithelialization. We also examined the neutrophilic inflammatory responses and neutrophil extracellular trap (NET)-osis at the wound sites after administration of α-mannan. The percent wound closure and re-epithelialization was significantly accelerated in dectin-2-knockout mice compared with wild-type mice on days 3 and 5 after wounding. In contrast, administration of α-mannan delayed wound closure in wild-type mice, and these responses were canceled in dectin-2-knockout mice. Furthermore, mice administered α-mannan, neutrophil infiltration was prolonged, and the expression of citrullinated histone, an indicator of NETosis, at the wound sites was accelerated. Administration of a neutrophil elastase inhibitor significantly improved the delayed wound healing caused by α-mannan. These results suggest that dectin-2 may have a deep impact on the skin wound healing process through regulation of neutrophilic responses.
Nicotine exposure induces the proliferation of oral cancer cells through the α7 subunit of the nicotinic acetylcholine receptor International-journal Peer-reviewed

Nishioka T, Tada H, Ibaragi S, Chen C, Sasano T

Biochemical and Biophysical Research Communications　509　(2)　514-520　2019/02
Publisher: Elsevier BV
DOI： 10.1016/j.bbrc.2018.12.154 　

ISSN： 0006-291X

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Oral cancer and smoking are closely related, because the oral cavity, which is the route of ingestion of tobacco smoke, is in direct contact with the oral mucosa. Nicotine, one of the components of tobacco, can diffuse rapidly to the central nervous system and is responsible for tobacco addiction. Nicotine is present in high concentrations in the bloodstream of smokers; while the addictive effects of this alkaloid have extensively been studied, its effect on tumorigenesis is not clear yet. Therefore, in this study, we examined the effect of nicotine on cell proliferation and the signaling pathways it activates. The human oral squamous cell carcinoma cell line HSC-2 was used as a model system. We demonstrated the correlation between nicotine and epidermal growth factor receptor (EGFR) signaling. Nicotine treatment induced HSC-2 cell proliferation and migration and the phosphorylation of EGFR. Furthermore, nicotine treatment activated the EGFR downstream effectors phosphatidylinositol-3 kinase/AKT and p44/42 mitogen-activated protein kinases (ERK), which, in turn, promoted cell proliferation. Overall, our study suggests that nicotine promotes cell growth and migration through epidermal growth factor (EGF) signaling and plays an important role in oral cancer progression.
Augmentation of Lipopolysaccharide-Induced Production of IL-1α and IL-1β in Mice Given Intravenous Zoledronate (a Nitrogen-Containing Bisphosphonate) and Its Prevention by Clodronate (a Non-nitrogen-containing Bisphosphonate). Peer-reviewed

Suzuki H, Bando K, Tada H, Kiyama T, Oizumi T, Funayama H, Sugawara S, Takahashi T, Endo Y

Biological and Pharmaceutical Bulletin　42　(2)　164-172　2019

DOI： 10.1248/bpb.b18-00408 　

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Bisphosphonates (BPs) bind strongly to bone and exhibit long-acting anti-bone-resorptive effects. Among BPs, nitrogen-containing BPs (N-BPs) have far stronger anti-bone-resorptive effects than non-N-BPs. However, N-BPs induce acute inflammatory reactions (fever, arthralgia and myalgia, etc.) after their first injection. The mechanisms underlying these side effects remain unclear. Zoledronate (one of the most potent N-BPs) is given intravenously to patients, and the side-effect incidence is reportedly the highest among N-BPs. Our murine experiments have clarified that (a) intraperitoneally injected N-BPs induce various inflammatory reactions, including a production of interleukin-1 (IL-1) (a typical inflammatory cytokine), and these inflammatory reactions are weak in IL-1-deficient mice, (b) subcutaneously injected N-BPs induce inflammation/necrosis at the injection site, (c) lipopolysaccharide (LPS; a cell-wall component of Gram-negative bacteria) and N-BPs mutually augment their inflammatory/necrotic effects, (d) the non-N-BP clodronate can reduce N-BPs' inflammatory/necrotic effects. However, there are few animal studies on the side effects of intravenously injected N-BPs. Here, we found in mice that (i) intravenous zoledronate exhibited weaker inflammatory effects than intraperitoneal zoledronate, (ii) in mice given intravenous zoledronate, LPS-induced production of IL-1α and IL-1β was augmented in various tissues, including bone, resulting in them increasing in serum, and (iii) clodronate (given together with zoledronate) prevented such augmentation and enhanced, slightly but significantly, zoledronate's anti-bone-resorptive effect. These results suggest that infection may be a factor promoting the acute inflammatory side effects of N-BPs via augmented production of IL-1 in various tissues (including bone), and that clodronate may be useful to reduce or prevent such side effects.
Cyclic Stretch Force Induces Periodontal Ligament Cells to Secrete Exosomes That Suppress IL-1β Production Through the Inhibition of the NF-κB Signaling Pathway in Macrophages. International-journal Peer-reviewed

Wang Z, Maruyama K, Sakisaka Y, Suzuki S, Tada H, Suto M, Saito M, Yamada S, Nemoto E

Frontiers in ImmunologyFrontiers in Immunology　10　1310-1310　2019

DOI： 10.3389/fimmu.2019.01310 　

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In the oral mechanical environment, periodontal ligament cells (PDL cells) contribute to maintaining periodontal tissue homeostasis. Recent studies showed that exosomes, which are small vesicles secreted by various types of cells, play a pivotal role in cell-to-cell communication in biological processes. We examined the secretion of exosomes from PDL cells stimulated with cyclic stretch and their role in the inflammatory response of macrophages using the human macrophage cell line THP-1 and human primary monocytes/macrophages. We prepared supernatants from human PDL cells (PDL-sup) stimulated with cyclic stretch. The treatment of macrophages with PDL-sup, but not PDL-sup from unstimulated PDL cells, inhibited the production of IL-1β in LPS/nigericin-stimulated macrophages. The pretreatment of PDL cells with GW4869, an inhibitor of exosome secretion, or siRNA for Rab27B, which controls exosome secretion, abrogated the inhibitory effects of PDL-sup. A transmission electron microscopy analysis demonstrated the existence of exosomes with diameters ranging between 30 and 100 nm in PDL-sup, suggesting that exosomes in PDL-sup contribute to this inhibition. An immunofluorescence microscopy analysis revealed that exosomes labeled with PKH67, a fluorescent dye, were incorporated by macrophages as early as 2 h after the addition of exosomes. Purified exosomes inhibited IL-1β production in LPS/nigericin-stimulated macrophages and the nuclear translocation of NF-κB as well as NF-κB p65 DNA-binding activity in LPS-stimulated macrophages, suggesting that exosomes suppress IL-1β production by inhibiting the NF-κB signaling pathway. Our results indicate that PDL cells in mechanical environments contribute to the maintenance of periodontal immune/inflammatory homeostasis by releasing exosomes.
Porphyromonas gingivalis induces the production of IL-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier International-journal Peer-reviewed

Tada H, Nishioka T, Takase A, Numazaki K, Bando K, Matsushita K

Cellular Microbiology　21　(3)　e12972　2019/01

DOI： 10.1111/cmi.12972 　

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Interleukin (IL)-31 is important for innate immunity in mucosal tissues and skin, and increased IL-31 expression participates in the pathogenesis of chronic inflammatory diseases affecting the skin, airways, lungs, and intestines. We investigated the contribution of mast cells to the induction of IL-31 production following infection with the periodontal pathogen, Porphyromonas gingivalis. We found that oral infection with P. gingivalis increased IL-31 expression in the gingival tissues of wild-type mice but not in those of mast cell-deficient mice. The P. gingivalis-induced IL-31 production by human mast cells occurred through the activation of the JNK and NF-κB signalling pathways and was dependent on the P. gingivalis lysine-specific protease gingipain-K. P. gingivalis infection induced IL-31 receptor α and oncostatin M receptor β expression in human gingival epithelial cells. Notably, the P. gingivalis-induced IL-31 production by mast cells led to the downregulation of claudin-1, a tight junction molecule, in gingival epithelial cells, resulting in an IL-31-dependent increase in the paracellular permeability of the gingival epithelial barrier. These findings suggest that IL-31 produced by mast cells in response to P. gingivalis infection causes gingival epithelial barrier dysfunction, which may contribute to the chronic inflammation observed in periodontitis.
MrgX2-mediated internalization of LL-37 and degranulation of human LAD2 mast cells Peer-reviewed

Murakami T, Suzuki K, Niyonsaba F, Tada H, Reich J, Tamura H, Nagaoka I

Molecular Medicine Reports　2018/10

DOI： 10.3892/mmr.2018.9532 　
Cyclic stretch negatively regulates IL-1β secretion through the inhibition of NLRP3 inflammasome activation by attenuating the AMP kinase pathway Peer-reviewed

Kentaro Maruyama, Yukihiko Sakisaka, Mizuki Suto, Hiroyuki Tada, Takashi Nakamura, Satoru Yamada, Eiji Nemoto

Frontiers in Physiology　9　(JUN)　802　2018/06/28

DOI： 10.3389/fphys.2018.00802 　

eISSN： 1664-042X
Periodontitis induced by bacterial infection exacerbates features of Alzheimer's disease in transgenic mice. International-journal Peer-reviewed

Ishida N, Ishihara Y, Ishida K, Tada H, Funaki-Kato Y, Hagiwara M, Ferdous T, Abdullah M, Mitani A, Michikawa M, Matsushita K

NPJ Aging and Mechanisms of Disease　3　15-15　2017

DOI： 10.1038/s41514-017-0015-x 　

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Periodontitis is a localized infectious disease caused by periodontopathic bacteria, such as Porphyromonas gingivalis. Recently, it has been suggested that bacterial infections may contribute to the onset and the progression of Alzheimer's disease (AD). However, we do not have any evidence about a causative relationship between periodontitis and AD. In this study, we investigated by using a transgenic mouse model of AD whether periodontitis evoked by P. gingivalis modulates the pathological features of AD. Cognitive function was significantly impaired in periodontitis-induced APP-Tg mice, compared to that in control APP-Tg mice. Levels of Amiloid β (Aβ) deposition, Aβ40, and Aβ42 in both the hippocampus and cortex were higher in inoculated APP-Tg mice than in control APP-Tg mice. Furthermore, levels of IL-1β and TNF-α in the brain were higher in inoculated mice than in control mice. The levels of LPS were increased in the serum and brain of P. gingivalis-inoculated mice. P. gingivalis LPS-induced production of Aβ40 and Aβ42 in neural cell cultures and strongly enhanced TNF-α and IL-1β production in a culture of microglial cells primed with Aβ. Periodontitis evoked by P. gingivalis may exacerbate brain Aβ deposition, leading to enhanced cognitive impairments, by a mechanism that involves triggering brain inflammation.
Porphyromonas gingivalis-induced IL-33 down-regulates hCAP-18/LL-37 production in human gingival epithelial cells Peer-reviewed

Tada H, Shimizu T, Matsushita K, Takada H

Biomedical Research　38　(3)　167-173　2017

DOI： 10.2220/biomedres.38.167 　

ISSN： 0388-6107

eISSN： 1880-313X
Increases in IL-33 production by fimbriae and lipopeptide from Porphyromonas gingivalis in mouse bone marrow-derived dendritic cells via Toll-like receptor 2 Peer-reviewed

Tada H, Suzuki R, Nemoto E, Shimauchi H, Matsushita K, Takada H

Biomedical Research　38　(3)　189-195　2017

DOI： 10.2220/biomedres.38.189 　

ISSN： 0388-6107

eISSN： 1880-313X
Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells International-journal Peer-reviewed

Tada H, Matsuyama T, Nishioka T, Hagiwara M, Kiyoura Y, Shimauchi H, Matsushita K

PLOS ONE　11　(4)　e0152794-TH010711　2016/04

DOI： 10.1371/journal.pone.0152794 　

ISSN： 1932-6203
Vitamin D₃ analog maxacalcitol (OCT) induces hCAP-18/LL-37 production in human oral epithelial cells Peer-reviewed

Tada H, Shimizu T, Nagaoka I, Takada H

Biomedical Research　37　(3)　199-205　2016

DOI： 10.2220/biomedres.37.199 　

ISSN： 0388-6107

eISSN： 1880-313X
Vinculin and Rab5 Complex is Requited for Uptake of Staphylococcus aureus and Interleukin-6 Expression Peer-reviewed

Hagiwara M, Kokubu E, Sugiura S, Komatsu T, Tada H, Isoda R, Tanigawa N, Kato Y, Ishida N, Kobayashi K, Nakashima M, Ishihara K, Matsushita K

PLOS ONE　9　(1)　e87373-TH010711　2014/01

DOI： 10.1371/journal.pone.0087373 　

ISSN： 1932-6203
POT1b regulates phagocytosis and NO production by modulating activity of the small GTPase Rab5 Peer-reviewed

Hagiwara M, Komatsu T, Sugiura S, Isoda R, Tada H, Tanigawa N, Kato Y, Ishida N, Kobayashi K, Matsushita K

Biochemical and Biophysical Research Communications　439　(3)　413-417　2013/09

DOI： 10.1016/j.bbrc.2013.08.018 　

ISSN： 0006-291X
Acacetin inhibits expression of E-selectin on endothelial cells through regulation of the MAP kinase signaling pathway and activation of NF-kappa B Peer-reviewed

Tanigawa, N, Hagiwara, M, Tada, H, Komatsu, T, Sugiura, S, Kobayashi K, Kato, Y, Ishida, N, Nishida, K, Ninomiya, M, Koketsu, M, Matsushita, K

Immunopharmacology and Immunotoxicology　35　(4)　471-477　2013/08

DOI： 10.3109/08923973.2013.811596 　

ISSN： 0892-3973
Extracellular phosphate increases bone morphogenetic protein-2 expression in human dental pulp cells and human periodontal ligament cells Peer-reviewed

Nemoto E, Tada H, Shimauchi H

Interface Oral Health Science 2011　143-144　2012/01/01
Publisher: Springer Japan
DOI： 10.1007/978-4-431-54070-0_35 　
Phosphate increases bone morphogenetic protein-2 expression through cAMP-dependent protein kinase and ERK1/2 pathways in human dental pulp cells Peer-reviewed

Tada H, Nemoto E, Foster BL, Somerman MJ, Shimauchi H

BONE　48　(6)　1409-1416　2011/06

DOI： 10.1016/j.bone.2011.03.675 　

ISSN： 8756-3282
Elevated extracellular calcium increases expression of bone morphogenetic protein-2 gene via a calcium channel and ERK pathway in human dental pulp cells Peer-reviewed

Tada H, Nemoto E, Kanaya S, Hamaji N, Sato H, Shimauchi H

Biochemical and Biophysical Research Communications　394　(4)　1093-1097　2010/04

DOI： 10.1016/j.bbrc.2010.03.135 　

ISSN： 0006-291X
Transitions in Oral and Intestinal Microflora Composition and Innate Immune Receptor-Dependent Stimulation during Mouse Development Peer-reviewed

Hasegawa M, Osaka T, Tawaratsumida K, Yamazaki T, Tada H, Chen GY, Tsuneda S, Nunez G, Inohara N

Infection and Immunity　78　(2)　639-650　2010/02

DOI： 10.1128/IAI.01043-09 　

ISSN： 0019-9567
Nucleotide-binding Oligomerization Domain-Like Receptor Signaling Enhances Dendritic Cell-Mediated Cross-priming in vivo. Peer-reviewed

Asano J, Tada H, Onai N, Sato T, Horie Y, Fujimoto Y, Fukase K, Suzuki A, Mak TW, Ohteki T

The Journal of Immunology　184　(2)　736-745　2010/01

DOI： 10.4049/jimmunol.0900726 　

ISSN： 1550-6606

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Nucleotide oligomerization binding domain (Nod)-like receptors are critical cytosolic sensors for the recognition of bacterial peptidoglycan. However, their role in the induction of dendritic cell (DC)-mediated cross-priming remains unclear. In this study, we demonstrate that injecting ligands for Nod1 and Nod2 along with Ag into wild-type mice significantly enhanced the cross-priming of Ag-specific CD8+ T cells by CD8alpha+ DCs, as assessed from the expansion of IFN-gamma+ CD8+ T cells, CTL activity against Ag-pulsed targets, and the rejection of transplanted tumors expressing the cognate Ag. The enhancement of CD8alpha+ DC-mediated cross-priming was likely due to the upregulation of Ag cross-presentation and of costimulatory molecules. Our findings collectively indicate that Nod1/2 signaling is critical for the optimal induction of DC cross-priming in vivo, which may offer an alternative therapeutic pathway in cancer and hosts refractory to TLR signals or paralyzed by viral evasion strategy.
Essential roles of DC-derived IL-15 as a mediator of inflammatory responses in vivo Peer-reviewed

Ohteki T, Tada H, Ishida K, Sato T, Maki C, Yamada T, Hamuro J, Koyasu S

The Journal of Experimental Medicine　203　(10)　2329-2338　2006/10

DOI： 10.1084/jem.20061297 　

ISSN： 0022-1007
Interleukin 15-dependent crosstalk between conventional and plasmacytoid dendritic cells is essential for CpG-induced immune activation Peer-reviewed

Kuwajima S, Sato T, Ishida K, Tada H, Tezuka H, Ohteki T

Nature Immunology　7　(7)　740-746　2006/07

DOI： 10.1038/ni1348 　

ISSN： 1529-2908
Synergistic Effect of Nod1 and Nod2 Agonists with Toll-Like Receptor Agonists on Human Dendritic Cells To Generate Interleukin-12 and T Helper Type 1 Cells Peer-reviewed

Tada H, Aiba S, Shibata K, Ohteki T, Takada H

Infection and Immunity　73　(12)　7967-7976　2005/12

DOI： 10.1128/iai.73.12.7967-7976.2005 　

ISSN： 0019-9567

eISSN： 1098-5522
Expression of CD73/ecto-5'-nucleotidase on human gingival fibroblasts and contribution to the inhibition of interleukin-1alpha-induced granulocyte-macrophage colony stimulating factor production International-journal Peer-reviewed

Nemoto E, Kunii R, Tada H, Tsubahara T, Ishihata H, Shimauchi H

Journal of Periodontal Research　39　(1)　10-19　2004/02

DOI： 10.1111/j.1600-0765.2004.00698.x 　

ISSN： 0022-3484

eISSN： 1600-0765
Proteolysis of ICAM-1 on human oral epithelial cells by gingipains Peer-reviewed

Tada H, Sugawara S, Nemoto E, Imamura T, Potempa J, Travis J, Shimauchi H, Takada H

Journal of Dental Research　82　(10)　796-801　2003/10

ISSN： 0022-0345
Expression of IL-2 receptor β and γ chains by human gingival fibroblasts and up-regulation of adhesion to neutrophils in response to IL-2 Peer-reviewed

Ozawa, A, Tada, H, Tamai, R, Uehara, A, Watanabe, K, Yamaguchi, T, Shimauchi, H, Takada, H, Sugawara, S

Journal of Leukocyte Biology　74　(3)　352-359　2003/09

DOI： 10.1189/jlb.0103044 　

ISSN： 0741-5400
Proteolysis of ICAM-1 on human oral epithelial cells by cysteine proteinase, (Gingipains) from Porphyromonas gingivalis leading to down-regulation of neutrophil adhesion. International-journal International-coauthorship Peer-reviewed

Tada H, Sugawara S, Nemoto E, Takahashi N, Imamura T, Potempa J, Travis J, Shimauchi H, Takada H

Journal of Dental Research　82　(10)　B41-B41　2003/06

DOI： 10.1177/154405910308201007 　

ISSN： 0022-0345
Disruption of CD40/CD40 ligand interaction with cleavage of CD40 on human gingival fibroblasts by human leukocyte elastase resulting in down-regulation of chemokine production International-journal Peer-reviewed

Nemoto E, Tada H, Shimauchi H

Journal of Leukocyte Biology　72　(3)　538-545　2002/09

ISSN： 0741-5400
Proteolysis of CD14 on human gingival fibroblasts by arginine-specific cysteine proteinases from Porphyromonas gingivalis leading to down-regulation of lipopolysaccharide-induced interleukin-8 production International-journal International-coauthorship Peer-reviewed

Tada H, Sugawara S, Nemoto E, Takahashi N, Imamura T, Potempa J, Travis J, Shimauchi H, Takada H

Infection and Immunity　70　(6)　3304-3307　2002/06

DOI： 10.1128/IAI.70.6.3304-3307.2002 　

ISSN： 0019-9567
Saccharomyces cerevisiae- and Candida albicans-derived mannan induced production of tumor necrosis factor alpha by human monocytes in a CD14-and Toll-like receptor 4-dependent manner International-journal Peer-reviewed

Tada H, Nemoto E, Shimauchi H, Watanabe T, Mikami T, Matsumoto T, Ohno N, Tamura H, Shibata K, Akashi S, Miyake K, Sugawara S, Takada H

Microbiology and Immunology　46　(7)　503-512　2002

DOI： 10.1111/j.1348-0421.2002.tb02727.x 　

ISSN： 0385-5600
Cleavage of CD14 on human gingival fibroblasts cocultured with activated neutrophils is mediated by human leukocyte elastase resulting in down-regulation of lipopolysaccharide-induced IL-8 production International-journal Peer-reviewed

Nemoto E, Sugawara S, Tada H, Takada H, Shimauchi H, Horiuchi H

The Journal of Immunology　165　(10)　5807-5813　2000/11

ISSN： 0022-1767
Proteolysis of human monocyte CD14 by cysteine proteinases (Gingipains) from Porphyromonas gingivalis leading to lipopolysaccharide hyporesponsiveness International-journal Peer-reviewed

Sugawara S, Nemoto E, Tada H, Miyake K, Imamura T, Takada H

The Journal of Immunology　165　(1)　411-418　2000/07

ISSN： 0022-1767

eISSN： 1550-6606

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Misc. 47

歯周炎におけるPorphyromonas gingivalisジンジパインと好中球細胞外トラップによる血液脳関門破綻と認知機能低下

多田浩之, 根本英二, 松下健二

第67回秋季日本歯周病学会学術大会　2024/10
歯周病における骨芽細胞の役割: Filifactor alocis による炎症誘導と破骨細胞分化促進

鶴田侑万, 多田浩之, 菅原俊二

令和6年度スチューデント・クリニシャン・リサーチ・プログラム(SCRP)日本代表選抜大会　2024/08
歯周病における歯周病原細菌と好中球による血液脳関門破綻と認知機能低下 Invited

多田浩之

第31回内毒素・LPS研究会　2024/06
歯周病原細菌プロテアーゼとNETsのクロストークによる脳機能障害

多田浩之, 西岡貴志, 松下健二

第28回日本エンドトキシン・自然免疫研究会　2023/12
歯周病マウスモデルにおけるPorphyromonas gingivalisと好中球による脳機能障害の検討

リュウドウシン, 多田浩之, 西岡貴志, 松下健二, 菅原俊二

2023/09
Neutrophil extracellular trapsのdouble-stranded DNAは破骨細胞分化を制御する

沼崎研人, 西岡貴志, 松下健二, 多田浩之

第27回日本エンドトキシン・自然免疫研究会　2022/11
Porphyromonas gingivalis線毛はLPSによるヒト単球のインターロイキン-6産生を相乗的に誘導する

遠山学, 多田浩之, 沼崎研人, 松下健二, 菅原俊二

第64回歯科基礎医学会学術大会　2022/09
The functional role of neutrophil extracellular traps in RANKL-induced osteoclastogenesis

Kento Numazaki, Hiroyuki Tada, Kenji Matsushita, Itaru Mizoguchi, Shunji Sugawara

2022/09
Porphyromonas gingivalis gingipains-mediated degradation of PAI-1 leads to delayed wound healing responses in human endothelial cells

Hiroyuki Tada, Takashi Nishioka, Kenji Matsushita, Shunji Sugawara

2022/09
Exacerbation of inflammation in periodontitis: Porphyromonas gingivalis fimbriae induce synergistic interleukin-6 production in human monocytes

Manabu Toyama, Hiroyuki Tada, Shunji Sugawara

2022
Proteolysis of PAI-1 by P. gingivalis gingipains leading to delayed wound healing responses in endothelial cells

Hiroyuki Tada, Li-Ting Song, Takahisa Imamura, Jan Potempa, Kenji Matsushita, Shunji Sugawara

16th Meeting of the International Endotoxin and Innate Immunity Society　2021/10
Porphyromonas gingivalisジンジパインによる血管内皮細胞のPAI-1分解と創傷治癒遅延

2021/10
Hericium erinaceus ethanol extracts have endotoxin-neutralizing activity

Hiraku Osawa, Sakura Onoue, Kazuyoshi Kawahara, Kenji Matsushita, Hiroyuki Tada

第94回日本細菌学会総会　2021/03
P. gingivalis and F. nucleatum augment E. coli LPS-induced IL-6 production by human monocytes

Yuya Sakamoto, Sakura Onoue, Kazuyoshi Kawahara, Kenji Matsushita, Hiroyuki Tada

第94回日本細菌学会総会　2021/03
Proteolysis of PAI-1 in human endothelial cells by gingipains from Porphyromonas gingivalis

Liting Song, Kenji Matsushita, Hiroyuki Tada

第94回日本細菌学会総会　2021/03
Cysteine proteinases from Porphyromonas gingivalis induces the production of IL-31 by mast cells, resulting in downregulation of claudin-1 in gingival epithelial cells

Hiroyuki Tada, Kenji Matsushita, Shunji Sugawara

第48回日本免疫学会学術集会　2019/12
Fusobacterium nucleatum感染によるマスト細胞からの細胞外トラップ産生と炎症誘導

多田浩之, 西岡貴志, 松下健二, 菅原俊二

第61回歯科基礎医学会学術大会　2019　2019/10

ISSN： 2187-9109
Porphyromonas gingivalisジンジパインによりマスト細胞が産生するIL-31は、歯肉上皮細胞のclaudin-1発現を抑制しバリア破綻を誘導する

多田浩之, 西岡貴志, 沼崎研人, 根本英二, 松下健二, 菅原俊二

第73回日本細菌学会東北支部会　2019/08
Fusobacterium nucleatum induces the production of extracellular traps by human mast cells, resulting in inflammatory responses

多田浩之, 西岡貴志, 松下健二, 尾之上さくら, 川原一芳

第25回日本エンドトキシン・自然免疫研究会　2019

ISSN： 2434-1177
Porphyromonas gingivalisによるマスト細胞由来interleukin-31を介した歯肉上皮細胞のclaudin-1ダウンレギュレーション作用

多田浩之, 西岡貴志, 根本英二, 松下健二

第149回日本歯科保存学会2018年度秋季学術大会　2018/11
歯周病原細菌によるヒトマスト細胞からの細胞外トラップ産生と炎症誘導

多田浩之, 西岡貴志, 松下健二

第24回日本エンドトキシン・自然免疫研究会　2018/11
Neutrophil extracellular trapsによるヒト血管内皮細胞のICAM-1発現誘導

米満由奈帆, 松下健二, 根本英二, 多田浩之

第61回秋季日本歯周病学会学術大会　2018/10
Fusobacterium nucleatumによるマスト細胞からのextracellular traps産生誘導

石山莉奈, 松下健二, 根本英二, 多田浩之

第61回秋季日本歯周病学会学術大会　2018/10
P. gingivalis感染によりマスト細胞から産生されたIL‐31はclaudin‐1発現抑制を介して歯肉上皮バリア破綻を誘導する

多田浩之, 沼崎研人, 西岡貴志, 松下健二, 菅原俊二

2018/09

ISSN： 2187-9109
歯周病におけるneutrophil extracellular traps産生と血管内皮細胞の炎症誘導

多田浩之, 西岡貴志, 松下健二, 尾之上さくら, 川原一芳

2017/12
歯周病原細菌感染によるNETs産生は血管内皮細胞における炎症反応を増悪させる

多田浩之, 松下健二, 根本英二

日本歯周病学会60周年記念京都大会　2017/10
Neutrophil extracellular trapsによるヒト血管内皮細胞のDel-1産生抑制

多田浩之, 西岡貴志, 松下健二, 菅原俊二

第59回歯科基礎医学会学術大会　2017　2017/09
Publisher: (一社)歯科基礎医学会
ISSN： 2187-2333
Fusobacterium nucleatumによる好中球のneutrophil extracellular traps産生を介した炎症反応の増悪

多田浩之, 松下健二

第60回春期日本歯周病学会学術大会　2017/05
Fusobacterium nucleatum induces the production of NETs-associated MIF by human neutrophils

Hiroyuki Tada

第90回日本細菌学会総会　2017/03
The 2017 Japan-NIH Joint Symposium

Hiroyuki Tada, Takashi Nishioka

The 2017 Japan-NIH Joint Symposium　2017/02
歯周病関連細菌による好中球のneutrophil extracellular traps産生を介した炎症反応の誘導

多田浩之, 沼崎研人, 西岡貴志, 松下健二, 高田春比古

2016/12
Fusobacterium nucleatumによるヒト好中球からのneutrophil extracellular traps誘導

沼崎研人, 西岡貴志, 松下健二, 多田浩之

2016/08
Publisher: (一社)歯科基礎医学会
ISSN： 2187-2333
Porphyromonas gingivalisによるヒト肥満細胞のIL-31誘導は歯肉上皮細胞のバリア機能を低下させる

多田浩之, 松下健二, 高田春比古

第59回春期日本歯周病学会学術大会　2016/05
Lactobacillusペプチドグリカンの可溶化フラグメントによるオートファジー誘導

多田浩之, 川原一芳, 高田春比古

第89回日本細菌学会総会　2016/03
Porphyromonas gingivalisジンジパインによるヒトマスト細胞からのIL-31産生誘導

多田浩之, 高瀬彩, 松下健二, 高田春比古

第21回日本エンドトキシン・自然免疫研究会　2015/12
Porphyromonas gingivalis fimbriaeによる樹状細胞のクロスプレゼンテーション誘導

2015/09
Porphyromonas gingivalisはヒトマスト細胞からIL-31産生を誘導する

高瀬彩, 多田浩之, 西岡貴志, 松下健二, 高田春比古

2015/09
Publisher: (一社)歯科基礎医学会
ISSN： 2187-2333
Porphyromonas gingivalisによるIL-33を介したLL/37/CAP-18ダウンレギュレーション作用

2015/08
Porphyromonas gingivalisによるヒトマスト細胞からのinterleukin-31産生誘導

多田浩之, 高瀬彩, 西岡貴志, 島内英俊, 松下健二, 高田春比古

2015/06
Publisher: (NPO)日本歯科保存学会
Porphyromonas gingivalisジンジパインによるIL-33誘導はヒト歯肉上皮細胞のCAP-18/LL-37産生を抑制する

2015/05
Possible roles of IL-33 in periodontal diseases: Porphyromonas gingivalis induced IL-33 in human gingival epithelial cells Invited

Hiroyuki Tada, Haruhiko Takada

Interface Oral Health Science 2014: Innovative Research on Biosis-Abiosis Intelligent Interface　2015/01/01
Publisher: Springer Japan
DOI： 10.1007/978-4-431-55192-8_25 　
Porphyromonas gingivalisによるヒト歯肉上皮細胞のLL-37発現誘導はIL-33により下方制御される

多田浩之, 松下健二, 高田春比古

第56回歯科基礎医学会学術大会　2014/09
Porphyromonas gingivalisはヒト歯肉上皮細胞におけるIL-33発現を誘導する

多田浩之, 松山孝司, 清浦有祐, 島内英俊, 松下健二

第67回日本細菌学会東北支部総会　2013/08
Porphyromonas gingivalis由来fimbriaeおよびリポペプチドによる樹状細胞からのIL-33発現誘導

多田浩之

第56回日本歯周病学会春期学術大会　2013/05
IL-15による炎症反応の制御

樗木俊聡, 多田浩之

感染・炎症・免疫, 37(1)　10-16　2007/10
樹状細胞からのIL-15生産と炎症

多田浩之, 樗木俊聡

臨床免疫・アレルギー科, 48(3)　340-346　2007/06
自然免疫と獲得免疫の基礎：自然免疫と感染免疫における樹状細胞の役割

多田浩之, 樗木俊聡

最新医学 60　597-604　2005/11

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Books and Other Publications 17

腸内細菌となかよく生きて腸までとどく薬学管理口腔細菌叢のはなし

多田浩之

薬局（南山堂）　2024/05
歯周病におけるPorphyromonas gingivalisと好中球細胞外トラップによる脳機能障害の影響

多田浩之

エンドトキシン・自然免疫研究25　2024
Neutrophil extracellular traps in periodontal disease and their relationship to systemic disease

Hiroyuki Tada

2021/12
歯周病原細菌に対する自然免疫応答がもたらす慢性炎症と生体バリア破綻

多田浩之

エンドトキシン・自然免疫研究23, 医学図書出版株式会社　2020
Fusobacterium nucleatumによるマスト細胞の細胞外トラップ放出と炎症誘導

多田浩之, 西岡貴志, 松下健二, 尾之上さくら, 川原一芳

エンドトキシン・自然免疫研究22, 医学図書出版株式会社　2019
歯周病におけるneutrophil extracellular traps産生と血管内皮細胞の炎症誘導

多田浩之, 西岡貴志, 松下健二, 尾之上さくら, 川原一芳

2018
歯周病関連細菌による好中球からのneutrophil extracellular traps産生を介した炎症反応の誘導

多田浩之, 沼崎研人, 西岡貴志, 松下健二, 高田春比古

エンドトキシン・自然免疫研究20, 医学図書出版株式会社　2017
Porphyromonas gingivalisジンジパインによるヒトマスト細胞からのIL-31産生誘導

Tada, H, Takase, A, Matsushita, K, Takada, H

2016
Porphyromonas gingivalisジンジパインによるヒト歯肉上皮細胞のIL-33誘導を介したCAP18/LL-37ダウンレギュレーション機構

Tada, H, Matsushita, K, Matsuyama, T, Nagaoka, I, Takada, H

2015
Periodontal diseases as a possible risk factor for Alzheimer’s disease.

Ishida, N, Ishihara, N, Ishida, K, Tada, H, Kato, Y, Isoda, R, Hagiwara, M, Michikawa, M, Noguchi, T, Matsushita, K

Interface Oral Health Science 2014, Springer　2014
Possible roles of IL-33 in periodontal diseases: Porphyromonas gingivalis induced IL-33 in human gingival epithelial cells.

Tada, H, Shimauchi, H, Takada, H, Matsushita, K

Interface Oral Health Science 2014, Springer　2014
Porphyromonas gingivalisジンジパインによるヒト歯肉上皮細胞におけるIL-33発現誘導

多田浩之

エンドトキシン・自然免疫研究15, 医学図書出版株式会社　2012
Extracellular phosphate increases bone morphogenetic protein-2 expression in human dental pulp cells and human periodontal ligament cells.

Nemoto, E, Tada, H, Shimauchi, H

Interface Oral Health Science 2011, Springer　2011
IL-15による炎症反応の制御

樗木俊聡, 多田浩之

感染・炎症・免疫, 医学の門社　2007
樹状細胞からのIL-15生産と炎症

多田浩之, 樗木俊聡

臨床免疫・アレルギー科, 科学評論社　2007
IL-12関連サイトカインによる免疫調節機構

多田浩之, 樗木俊聡

Annual Review免疫2006, 中外医学社　2006
自然免疫と獲得免疫の基礎: 自然免疫と感染免疫における樹状細胞の役割

多田浩之, 樗木俊聡

最新医学「免疫と疾患（前篇）」, 最新医学社　2005

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Presentations 11

口腔と全身のネットワーク〜脈管系から生命現象を理解する〜歯周病原細菌による生体バリア破綻と血管修復障害 Invited

多田浩之

第64回歯科基礎医学会学術大会日本学術会議シンポジウム　2022/09/17
口腔細菌叢から全身の健康を科学する歯周病原細菌による自然免疫応答と生体バリア破綻 Invited

多田浩之

第18回日本抗加齢医学会総会シンポジウム　2018/05/26
Periodontal bacteria induce the production of MIF-associated neutrophil extracellular traps by human neutrophils International-presentation

Tada H, Nishioka T

The 2017 Japan-NIH Joint Symposium　2017/02/16
<I>Porphyromonas gingivalis</I-induced production of IL-31 by human mast cells resulting in dysfunction of gingival epithelial barrier International-presentation

Tada H, Takase A, Nishioka T, Matsushita K, Takada H

Innovative Research for Biosis-Abiosis Intelligent Interface Symposium　2016/01/18
Periodontitis Induced by Bacterial Infection Exacerbates Features of Alzheimer's disease in Transgenic Mice. International-presentation

Ishida, N, Ishihara, Y, Ishida, K, Tada, H, Kato, Y, Isoda, R, Hagiwara, M, Michikawa, M, Noguchi, T, Matsushita, K

Innovative Research for Biosis-Abiosis Intelligent Interface Symposium　2014/01/20
Vinculin: a Novel Rab5-binding protein required for internalization of Staphyrococcus aureus to nonphagocytic cells. International-presentation

Hagiwara, M, Kokubu, E, Sugiura, S, Komatsu, T, Tada, H, Isoda, R, Tanigawa, N, Kato, Y, Ishida, N, Kobayashi, K, Jingshu, W, Nakashima, M, Ishihara, K, Matsushita, K

Innovative Research for Biosis-Abiosis Intelligent Interface Symposium　2014/01/20
Increasing expression of interleukin-33 by Porphyromonas gingivalis gingipains in human gingival epithelial cells. International-presentation

Tada, H, Shimauchi, H, Matsushita, K

Innovative Research for Biosis-Abiosis Intelligent Interface Symposium　2014/01/20
ジンジパインによるアレルギー性サイトカイン誘導をターゲットとしたアレルギー疾患の制御 Invited

多田浩之

日本歯科医学会第29回「歯科医学を中心とした総合的な研究を推進する集い」　2014/01/12
Gingipains from Porphyromonas gingivalis enhance interleukin-33 expression in human gingival epithelial cells. International-presentation

Tada, H, Matsuyama, T, Kiyoura, Y, Shimauchi, H, Matsushita, K

NIH Tohoku University JSPS Symposium　2013/05/09
Essential roles of dendritic cell-derived IL-15 as a mediator of inflammatory responses in vivo. International-presentation Invited

TADA Hiroyuki

COE International Seminar by Yourng Scientists 2007　2007
歯周病原細菌に対する自然免疫応答がもたらす慢性炎症と生体バリア破綻 Invited

多田浩之

第25回日本エンドトキシン・自然免疫研究会最優秀賞受賞講演　2019/11/29

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Research Projects 24

GFPマウス歯胚移植における歯根膜再生メカニズムの解明

中村恵

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

Category: 基盤研究(C)

Institution: 東北大学

2021/04 - 2024/03
チタンに制菌性を与える合金化元素を選別し、制菌性強化型インプラント合金を開発する

高橋正敏

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

Category: 基盤研究(C)

Institution: 東北大学

2021/04 - 2024/03
口腔細菌叢・歯周病原細菌を標的とした認知症対策の可能性の検討

松下健二

Offer Organization: 文部科学省

System: 科学研究費基盤研究(B)

Category: 基盤研究(B)

Institution: 国立長寿医療研究センター

2020/04 - 2023/03
NETsを起点とした口腔がん発生機序の解明~口腔細菌とニコチンのクロストーク~

西岡貴志

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

Category: 基盤研究(C)

Institution: 東北大学

2020/04 - 2023/03
活性型ビタミンD3を基軸とした口腔粘膜の免疫応答調節機構の解明

菅原俊二

Offer Organization: 文部科学省

System: 科学研究費基盤研究(B)

Category: 基盤研究(B)

Institution: 東北大学

2019/04 - 2022/03
歯周病原細菌による好中球細胞外トラップ誘導を基軸とした歯肉上皮バリア破綻の解明

多田浩之

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

Category: 基盤研究(C)

Institution: 東北大学

2019/04 - 2022/03
口腔の老化制御を基軸とした新しい口腔機能の維持・向上法の開発

松下健二

Offer Organization: 国立長寿医療研究センター

System: 長寿医療研究開発費

Institution: 東北大学

2020/04 - 2021/03
ヤマブシタケによるLPS中和作用を基軸とした血液脳関門ホメオスターシス制御

多田浩之

Offer Organization: 公益財団法人ホクト生物科学振興財団

System: 研究奨励金

Institution: 東北大学

2020/11 -
歯周病原細菌によるマスト細胞のIL-31を基軸とした歯肉上皮バリア破綻機序の解明 Competitive

多田浩之

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

2016/04 - 2019/03
アルツハイマー病の病態増悪に関与する歯周病分子機構の解明 Competitive

松下健二

Offer Organization: 文部科学省

System: 科学研究費基盤研究(B)

2014/04 - 2017/03
アレルギー誘導性サイトカインIL-33を基軸とした歯周炎増悪メカニズムの解明 Competitive

多田浩之

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

2013/04 - 2017/03
β-グルカンによるNETs結合性MIF産生をターゲットとした炎症性疾患の制御 Competitive

多田浩之

Offer Organization: 公益財団法人ホクト生物科学振興財団

System: 研究奨励金

2016/11 -
口腔レンサ球菌との共生を目指して：自然免疫の増強 Competitive

高田春比古

Offer Organization: 文部科学省

System: 科学研究費挑戦的萌芽研究

2013/04 - 2015/03
酸化的修飾タンパク質と歯周病病態との関連－アダクトミクス応用による網羅的解析－ Competitive

松下健二

Offer Organization: 文部科学省

System: 科学研究費挑戦的萌芽研究

2013/04 - 2015/03
乳酸菌糖脂質およびペプチドグリカンの自然免疫活性化における役割 Competitive

川原一芳

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

2012/04 - 2015/03
歯周病原細菌によるDC-SIGNを介したクロスプライミング誘導機構の解明 Competitive

多田浩之

Offer Organization: 文部科学省

System: 科学研究費若手研究(B)

2011/04 - 2013/03
Wntシグナル制御を軸としたセメント質再生法の基盤構築 Competitive

根本英二

Offer Organization: 文部科学省

System: 科学研究費基盤研究(B)

2009/04 - 2012/03
細胞外カルシウムおよびリン酸感知機構を軸とした象牙質再生法の基盤構築 Competitive

根本英二

Offer Organization: 文部科学省

System: 科学研究費挑戦的萌芽研究

2009/04 - 2012/03
P. gingivalisによるDC-SIGNを介したTh1応答のエスケープ機構 Competitive

多田浩之

Offer Organization: 文部科学省

System: 科学研究費若手研究(B)

2009/04 - 2011/03
NOD1を介した免疫ホメオスタシスの調節 Competitive

多田浩之

Offer Organization: 文部科学省

System: 科学研究費基盤研究(C)

2007/04 - 2009/03
Porphyromonas gingivalisによる樹状細胞のDC-SIGNを介したTh1応答エスケープ機構 Competitive

多田浩之

Offer Organization: 公益財団法人武田科学技術振興財団

System: 医学系研究奨励

2009 -
自然免疫系における歯周病関連細菌のプロテアーゼを介したエスケープ機構 Competitive

多田浩之

Offer Organization: 文部科学省

System: 科学研究費特別研究員奨励費

2003/04 - 2006/03
Nodタンパク質の介する免疫応答 Competitive

多田浩之

Offer Organization: 公益財団法人上原記念生命科学財団

System: リサーチフェローシップ

2006 -
炎症性腸疾患における腸管粘膜のNodタンパク質を介した免疫応答の解明 Competitive

多田浩之

Offer Organization: 公益財団法人内藤記念科学振興財団

System: 海外留学留学助成金

2006 -

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Teaching Experience 19

Advanced Graduate Program for Future Medicine and Health Care　Tohoku University
学部全学教育：学問論演習　Tohoku University
学部全学教育：からだの生物学　Tohoku University
歯学部専門教育：合同講義　東北大学
歯学部専門教育：基礎研究実習　東北大学
歯学部専門教育：歯学基礎演習　東北大学
歯学部専門教育：口腔細菌学実習　東北大学
歯学部専門教育：細菌学実習　東北大学
歯学部専門教育：感染と免疫　東北大学
学部全学教育：基礎ゼミ　東北大学
学部全学教育：生命と自然　東北大学
歯学研究科修士課程：実験技術トレーニングコースⅠ〜Ⅲ（口腔微生物学）　東北大学
歯学研究科修士課程：歯学演習（口腔微生物学）　東北大学
歯学研究科修士課程：歯学特論（口腔微生物学）　東北大学
歯学研究科博士課程：実験技術トレーニングコースⅠ〜Ⅲ（口腔微生物学）　東北大学
歯学研究科博士課程：歯学演習（口腔微生物学）　東北大学
歯学研究科博士課程：歯学特論（口腔微生物学）　東北大学
医学部専門教育：基礎研究配属　秋田大学
医学部専門教育：免疫学　秋田大学

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Social Activities 4

微生物学・口腔微生物学講義

2018 - Present
微生物学・口腔微生物学講義

2016 - Present
微生物学・口腔微生物学講義

2013 - Present
歯周病と自然免疫

平成29年度春季学術講演会

2017/04/08 -