TY - JOUR
T1 - Oral infection of mice with Fusobacterium nucleatum results in macrophage recruitment to the dental pulp and bone resorption
AU - Johnson, Larry
AU - Almeida-da-Silva, Cássio Luiz Coutinho
AU - Takiya, Christina Maeda
AU - Figliuolo, Vanessa
AU - Rocha, Gustavo Miranda
AU - Weissmüller, Gilberto
AU - Scharfstein, Julio
AU - Coutinho-Silva, Robson
AU - Ojcius, David M.
N1 - Publisher Copyright:
© 2018 Chang Gung University
PY - 2018/6
Y1 - 2018/6
N2 - 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.
AB - 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.
KW - Dental
KW - Immunology
KW - Inflammation
KW - Innate immunity
KW - Periodontal disease
UR - http://www.scopus.com/inward/record.url?scp=85049328970&partnerID=8YFLogxK
U2 - 10.1016/j.bj.2018.05.001
DO - 10.1016/j.bj.2018.05.001
M3 - 文章
C2 - 30080658
AN - SCOPUS:85049328970
SN - 2319-4170
VL - 41
SP - 184
EP - 193
JO - Biomedical Journal
JF - Biomedical Journal
IS - 3
ER -