Toshiharu Abe

ORCID: 0000-0002-8810-4861
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About
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Research Areas
  • Oral microbiology and periodontitis research
  • Immune Response and Inflammation
  • Oral Health Pathology and Treatment
  • Streptococcal Infections and Treatments
  • HIV/AIDS oral health manifestations
  • Immunodeficiency and Autoimmune Disorders
  • Cell Adhesion Molecules Research
  • Hepatitis B Virus Studies
  • Protease and Inhibitor Mechanisms
  • Antimicrobial Peptides and Activities
  • Blood disorders and treatments
  • S100 Proteins and Annexins
  • Neonatal and Maternal Infections
  • Phagocytosis and Immune Regulation
  • Anthropological Studies and Insights
  • Pneumonia and Respiratory Infections
  • Asian Geopolitics and Ethnography
  • Pancreatitis Pathology and Treatment
  • Ocular Diseases and Behçet’s Syndrome
  • Psoriasis: Treatment and Pathogenesis
  • Advanced Drug Delivery Systems
  • Platelet Disorders and Treatments
  • dental development and anomalies
  • Inflammation biomarkers and pathways
  • Advanced Glycation End Products research

Aichi Gakuin University
2024

University of Pennsylvania
2012-2020

Oulu University Hospital
2020

University of Oulu
2020

University of Louisville
2012

Periodontitis is one of the most common human inflammatory diseases, yet mechanisms that drive immunopathology and could be therapeutically targeted are not well defined. Here, we demonstrate an expansion resident memory T helper 17 (TH17) cells in periodontitis. Phenocopying humans, TH17 expanded murine experimental periodontitis through local proliferation. Unlike homeostatic oral cells, which accumulate a commensal-independent interleukin-6 (IL-6)-dependent manner,...

10.1126/scitranslmed.aat0797 article EN Science Translational Medicine 2018-10-17

Abstract When excessively activated or deregulated, complement becomes a major link between infection and inflammatory pathology including periodontitis. This oral disease is associated with dysbiotic microbiota, leads to the destruction of bone other tooth-supporting structures, exerts an adverse impact on systemic health. We have previously shown that mice deficient either in C5a receptor (C5aR; CD88) TLR2 are highly similarly resistant periodontitis, suggesting cross-talk two receptors...

10.4049/jimmunol.1202339 article EN The Journal of Immunology 2012-10-24

Abstract Chronic periodontitis is induced by a dysbiotic microbiota and leads to inflammatory destruction of tooth-supporting connective tissue bone. The third component complement, C3, point convergence distinct complement activation mechanisms, but its involvement in was not previously addressed. We investigated this question using two animal species models, namely, C3-deficient or wild-type mice nonhuman primates (NHPs) locally treated with potent C3 inhibitor (the compstatin analog Cp40)...

10.4049/jimmunol.1400569 article EN The Journal of Immunology 2014-05-08

Del-1 is an endothelial cell-secreted anti-inflammatory protein. In humans and mice, expression inversely related to that of IL-17, which inhibits through hitherto unidentified mechanism(s). Here we show IL-17 downregulates human cell by targeting a critical transcription factor, C/EBPβ. Specifically, causes GSK-3β-dependent phosphorylation C/EBPβ, associated with diminished C/EBPβ binding the promoter suppressed expression. This inhibitory action can be reversed at GSK-3β level PI3K/Akt...

10.1038/ncomms9272 article EN cc-by Nature Communications 2015-09-16

The oral and intestinal host tissues both carry a heavy microbial burden. Although commensal bacteria contribute to healthy tissue structure function, their contribution health is poorly understood. A crucial component of periodontal the recruitment neutrophils tissue. To elucidate this process, gingival specific-pathogen-free germ-free wild-type mice CXCR2KO MyD88KO were examined for quantitative analysis CXCR2 chemoattractants (CXCL1, CXCL2). We show that does not require bacterial...

10.1111/cmi.12127 article EN Cellular Microbiology 2013-02-25

Developmental endothelial locus–1 (DEL-1) is an endogenous homeostatic regulator of osteoclasts that blocks inflammatory bone loss in nonhuman primates.

10.1126/scitranslmed.aac5380 article EN Science Translational Medicine 2015-09-30

B-lineage cells (B lymphocytes and plasma cells) predominate in the inflammatory infiltrate of human chronic periodontitis. However, their role disease pathogenesis factors responsible for persistence lesions are poorly understood. In this regard, two cytokines TNF ligand superfamily, a proliferation-inducing (APRIL) B-lymphocyte stimulator (BLyS), important survival, proliferation, maturation B cells. Thus, we hypothesized that APRIL and/or BLyS upregulated periodontitis contribute to...

10.4049/jimmunol.1500496 article EN The Journal of Immunology 2015-07-07

ABSTRACT Chronic periodontitis is a local inflammatory disease induced by dysbiotic microbiota and leading to destruction of the tooth-supporting structures. Microbial nucleic acids are abundantly present in periodontium, derived through release after phagocytic uptake microbes and/or from biofilm-associated extracellular DNA. Binding microbial DNA its cognate receptors, such as Toll-like receptor 9 (TLR9), can trigger inflammation. In this study, we utilized TLR9 knockout (TLR9 −/− ) mice...

10.1128/iai.00424-15 article EN Infection and Immunity 2015-05-12

Abstract The glycoprotein milk fat globule–epidermal growth factor 8 (MFG-E8) is expressed in several tissues and mediates diverse homeostatic functions. However, whether it plays a role bone homeostasis has not been established. In this study, we show for the first time, to our knowledge, that osteoclasts express are regulated by MFG-E8. Bone marrow–derived osteoclast precursors from MFG-E8–deficient (Mfge8−/−) mice underwent increased receptor activator of NF-κB ligand–induced...

10.4049/jimmunol.1400970 article EN The Journal of Immunology 2014-06-24

Triggering receptor expressed on myeloid cells-1 (TREM-1) is a modifier of local and systemic inflammation. There clinical evidence implicating TREM-1 in the pathogenesis periodontitis. However, cause-and-effect relationship has yet to be demonstrated, as underlying mechanism. The aim this study was elucidate role using murine ligature-induced periodontitis model.A synthetic antagonistic LP17 peptide or sham control microinjected locally into palatal gingiva ligated molar teeth.Mice treated...

10.3390/jcm8101579 article EN Journal of Clinical Medicine 2019-10-01

We have previously shown that the secreted glycoprotein milk fat globule epidermal growth factor 8 (MFG-E8) has anti-inflammatory and anti-osteoclastogenic properties. Our objective was to investigate potential of MFG-E8 as a diagnostic or therapeutic agent in periodontitis.Periodontitis induced non-human primates (NHPs) by placing ligatures around posterior teeth on both halves mandible for split-mouth design: one side treated with MFG-E8-Fc other Fc control. Disease assessed clinical...

10.1111/jcpe.12707 article EN Journal Of Clinical Periodontology 2017-02-16

Understanding the progression of periodontal tissue destruction is at forefront research. The authors aimed to capture dynamics gingival proteome during initiation and experimental (ligature-induced) periodontitis in mice. Pressure cycling technology (PCT), a recently developed platform that uses ultra-high pressure disrupt tissues, utilized achieve efficient reproducible protein extraction from ultra-small amounts tissues combination with liquid chromatography-tandem mass spectrometry (MS)....

10.1002/pmic.201900253 article EN PROTEOMICS 2019-12-27

Porphyromonas gingivalis (P. gingivalis), an important periodontal pathogen, has been reported to be involved in aspiration-induced pneumonia. Its virulence factors involve FimA and Mfa1 fimbriae, with diverse gene variants across strains, showing potential associations pathogenicity. In this study, we aimed develop a novel aspiration pneumonia mouse model by infecting the lungs two different fimbrial genotypes of P. strains ATCC 33277 1439 via oral route, addressing limitations existing...

10.2485/jhtb.33.99 article EN Journal of Hard Tissue Biology 2024-01-01
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