Cited by 382Oral microbiology and periodontitis researchPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

A dysbiotic microbiome triggers T H 17 cells to mediate oral mucosal immunopathology in mice and humans

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Dutzan, Nicolas, Kajikawa, Tetsuhiro, Abusleme, Loreto, Greenwell-Wild, Teresa, Zuazo, Carlos E., Ikeuchi, Tomoko, Brenchley, Laurie, Abe, Toshiharu +11 more·2018·Science Translational Medicine

Abstract

Combined patient and animal model studies implicate microbiota-triggered T H 17 cells as disease drivers and therapeutic targets in periodontitis.

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Crossref · 10.1126/scitranslmed.aat0797

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  • Studies using germ-free mice have demonstrated the role of diabetes in disrupting the equilibrium of the oral microbiota and confirmed the role of the oral microbiota in periodontal disease pathogenesis.

    “Studies using germ‐free mice have also been employed in the context of the oral microbiome, demonstrating the role of diabetes in disrupting the equilibrium of the oral microbiota50 and confirming the role of the oral microbiota in periodontal disease pathogenesis.51, 52”
  • Functions of immune networks within oral mucosa reflect the site-specific challenges faced within the oral cavity; they contribute to homeostasis in response to masticatory forces and trigger immune responses to the development of pathologic microbial communities.

    “In line with the role of oral mucosa as a physiological barrier, the functions of immune networks within this mucosa reflect the site‐specific challenges faced within the oral cavity. For example, they contribute to homeostasis in response to masticatory forces and trigger immune responses to the development of pathologic microbial communities.52, 53”
  • Microbial dysbiosis is also necessary for additional inflammatory responses characteristic of periodontal disease, including local expansion of pathologic interleukin-17+/CD4+ T-helper (T-helper 17) cells.

    “Microbial dysbiosis is also necessary for additional inflammatory responses characteristic of periodontal disease, including local expansion of pathologic interleukin‐17+/CD4+ T‐helper (T‐helper 17) cells.52”
  • The importance of commensal species to pathogenesis is further demonstrated by the requirement for commensal microbial communities in the instigation of disease by periodontal pathogens.

    “The importance of commensal species to pathogenesis is further demonstrated by the requirement for commensal microbial communities in the instigation of disease by periodontal pathogens.51, 52”
  • In an additional study, homeostatic T-helper 17 cells were induced by mechanical stimuli in a microbiome-independent manner, whereas periodontitis-associated T-helper 17 cells accumulated in a microbiome-dependent manner and required both interleukin-6 and interleukin-23.

    “homeostatic T‐helper 17 cells were found to be induced by mechanical stimuli in a microbiome‐independent manner, whereas periodontitis‐associated T‐helper 17 cells were found to accumulate in a microbiome‐dependent manner and to require both interleukin‐6 and interleukin‐23.”

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Authors
Dutzan, N., Kajikawa, T., Abusleme, L., Greenwell-Wild, T., Zuazo, C. E., Ikeuchi, T., Brenchley, L., Abe, T., Hurabielle, C., Martin, D., Morell, R. J., Freeman, A. F., Lazarevic, V., Trinchieri, G., Diaz, P. I., Holland, S. M., Belkaid, Y., Hajishengallis, G., & Moutsopoulos, N. M.
Affiliations
  • Oral Immunity and Inflammation Unit, NIDCR, NIH, Bethesda, MD 20892, USA.
  • University of Pennsylvania (US)
  • National Institutes of Health (US)
  • Genomics and Computational Biology Core, NIDCD, NIH, Bethesda, MD 20892, USA.
  • UConn Health (US)
Corresponding author
Moutsopoulos, Niki M.
Venue
Science Translational Medicine
Published
2018-10-17
Volume
10
Issue
463
ISSN
  • 1946-6234 (ISSN-L)
  • 1946-6242
OpenAlex
W2896857921
Cited by
382
References
58
Citations by year
2026: 38 · 2025: 46 · 2024: 49 · 2023: 46 · 2022: 47 · 2021: 70 · 2020: 57 · 2019: 28 · 2018: 1
FWCI
44.82
Type
journal article
Language
en
Open access
Locations
  • Science Translational Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Fondation pour la Recherche Médicale
  • NIAID (IRP)
  • NIDCR (Intramural, DE024153, DE026152)
  • NCI Intramural
  • La Roche-Posay
  • CEDEF
  • Philippe Foundation
  • fondation groupe pasteur mutualité
  • Société Française de Dermatologie
Topics
  • Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
dysbiosis, oral microbiota, Th17 cells, oral inflammation, periodontitis, oral immunity, targeted therapy
MeSH terms
Animals, Bacteria, Bone Resorption, Cell Differentiation, Humans, Inflammation, Mouth Mucosa, Neutrophils, Periodontitis, Interleukin-6, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Microbiota, Dysbiosis

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