Interferon activated gene 204 protects against bone loss in experimental periodontitis.
genetics
host modulation
inflammasome
inflammatory disease
periodontitis
Journal
Journal of periodontology
ISSN: 1943-3670
Titre abrégé: J Periodontol
Pays: United States
ID NLM: 8000345
Informations de publication
Date de publication:
Sep 2022
Sep 2022
Historique:
revised:
03
03
2022
received:
24
11
2021
accepted:
31
03
2022
pubmed:
12
4
2022
medline:
24
9
2022
entrez:
11
4
2022
Statut:
ppublish
Résumé
Periodontal destruction can be the result of different known and yet-to-be-discovered biological pathways. Recent human genetic association studies have implicated interferon-gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)-1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis. Periodontitis was induced in Ifi204 Ifi204-deficient mice> exhibited >20% higher alveolar bone loss than wild-type (WT) (P < 0.05), while no significant difference was found in Aim2 These findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.
Sections du résumé
BACKGROUND
Periodontal destruction can be the result of different known and yet-to-be-discovered biological pathways. Recent human genetic association studies have implicated interferon-gamma inducible protein 16 (IFI16) and absent in melanoma 2 (AIM2) with high periodontal interleukin (IL)-1β levels and more destructive disease, but mechanistic evidence is lacking. Here, we sought to experimentally validate these observational associations and better understand IFI16 and AIM2's roles in periodontitis.
METHODS
Periodontitis was induced in Ifi204
RESULTS
Ifi204-deficient mice> exhibited >20% higher alveolar bone loss than wild-type (WT) (P < 0.05), while no significant difference was found in Aim2
CONCLUSIONS
These findings support IFI16's role as a novel regulator of inflammatory cell trafficking to the periodontium that protects against bone loss and offers potential targets for the development of new periodontal disease biomarkers and therapeutics.
Identifiants
pubmed: 35404474
doi: 10.1002/JPER.21-0668
pmc: PMC9489626
mid: NIHMS1797263
doi:
Substances chimiques
Biomarkers
0
Ifi16 protein, mouse
0
Nuclear Proteins
0
Phosphoproteins
0
Interferon-gamma
82115-62-6
Interferons
9008-11-1
Cathepsin K
EC 3.4.22.38
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1366-1377Subventions
Organisme : NIAID NIH HHS
ID : R01 AI153265
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK093771
Pays : United States
Organisme : NIDCR NIH HHS
ID : K01 DE027087
Pays : United States
Organisme : NCATS NIH HHS
ID : KL2 TR002490
Pays : United States
Organisme : NCI NIH HHS
ID : K22 CA212030
Pays : United States
Informations de copyright
© 2022 American Academy of Periodontology.
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