Oral infection of mice with Fusobacterium nucleatum results in macrophage recruitment to the dental pulp and bone resorption

Larry Johnson, Cássio Luiz Coutinho Almeida-da-Silva, Christina Maeda Takiya, Vanessa Figliuolo, Gustavo Miranda Rocha, Gilberto Weissmüller, Julio Scharfstein, Robson Coutinho-Silva, David M. Ojcius*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

22 Scopus citations


Background: Fusobacterium nucleatum is a Gram-negative anaerobic bacterium associated with periodontal disease. Some oral bacteria, like Porphyromonas gingivalis, evade the host immune response by inhibiting inflammation. On the other hand, F. nucleatum triggers inflammasome activation and release of danger-associated molecular patterns (DAMPs) in infected gingival epithelial cells. Methods: In this study, we characterized the pro-inflammatory response to F. nucleatum oral infection in BALB/c mice. Western blots and ELISA were used to measure cytokine and DAMP (HMGB1) levels in the oral cavity after infection. Histology and flow cytometry were used to observe recruitment of immune cells to infected tissue and pathology. Results: Our results show increased expression and production of pro-inflammatory cytokines during infection. Furthermore, we observe that F. nucleatum infection leads to recruitment of macrophages in different tissues of the oral cavity. Infection also contributes to osteoclast recruitment, which could be involved in the observed bone resorption. Conclusions: Overall, our findings suggest that F. nucleatum infection rapidly induces inflammation, release of DAMPs, and macrophage infiltration in gingival tissues and suggest that osteoclasts may drive bone resorption at early stages of the inflammatory process.

Original languageEnglish
Pages (from-to)184-193
Number of pages10
JournalBiomedical Journal
Issue number3
StatePublished - 06 2018
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2018 Chang Gung University


  • Dental
  • Immunology
  • Inflammation
  • Innate immunity
  • Periodontal disease


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