Fusobacterium nucleatum dysregulates inflammatory cytokines and NLRP3 inflammasomes in oral cells.
Oral Dis
; 30(7): 4767-4781, 2024 10.
Article
em En
| MEDLINE
| ID: mdl-38409736
ABSTRACT
OBJECTIVE:
This study aimed to clarify the difference in Fusobacterium nucleatum (F. nucleatum) induced inflammatory cytokines and nod-like receptor protein 3 (NLRP3) inflammasomes dysregulation among three periodontal cells.METHODS:
Oral epithelial cells (HIOECs), THP-1 macrophages, and human gingival fibroblasts (HGFs) were exposed to F. nucleatum with/without adenosine triphosphate (ATP) and nigericin (Nig). Cell morphology was assessed by scanning electron microscopy. qRT-PCR, protein microarrays, and bioinformatic methods were used to evaluate the cytokines and their complex interplay. NLRP3 inflammasomes activation was detected by western blotting and ELISA.RESULTS:
F. nucleatum adhered to and invaded cells. In HIOECs, F. nucleatum enhanced interleukin (IL)-1α/1ß/6/10/13, TNF-α, and interferon (IFN)-γ expression. In THP-1 macrophages, F. nucleatum up-regulated IL-1α/1ß/6/10 and TNF-α levels. In HGFs, F. nucleatum increased IL-6 levels. F. nucleatum and ATP synergistically boosted IFN-γ level in THP-1 macrophages and IL-13 level in HGFs. IL-1α/1ß/6, and TNF-α served as epicenters of the inflammatory response. Additionally, F. nucleatum activated NLRP3 inflammasomes in HIOECs, and ATP/Nig boosted the activation. F. nucleatum also triggered NLRP3 inflammasomes in THP-1 macrophages, but in HGFs, only NLRP3 and caspase-1 levels were elevated.CONCLUSION:
F. nucleatum infiltrated periodontal supporting cells and dysregulated inflammatory cytokines and NLRP3 inflammasomes.Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Citocinas
/
Fusobacterium nucleatum
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Inflamassomos
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Fibroblastos
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Proteína 3 que Contém Domínio de Pirina da Família NLR
/
Gengiva
Limite:
Humans
Idioma:
En
Revista:
Oral Dis
/
Oral dis
/
Oral diseases
Assunto da revista:
ODONTOLOGIA
Ano de publicação:
2024
Tipo de documento:
Article