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Halofuginone functions as a therapeutic drug for chronic periodontitis in a mouse model.

Abstract
Periodontitis is an inflammatory disease caused by host immune response, resulting in a loss of periodontium and alveolar bone. Immune cells, such as T cells and macrophages, play a critical role in the periodontitis onset. Halofuginone, a natural quinazolinone alkaloid, has been shown to possess anti-fibrosis, anti-cancer, and immunomodulatory properties. However, the effect of halofuginone on periodontitis has never been reported. In this study, a ligature-induced mice model of periodontitis was applied to investigate the potential beneficial effect of halofuginone on periodontitis. We demonstrated that the administration of halofuginone significantly reduced the expression levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in vivo, and markedly suppressed immune cell infiltration into the infected sites. Furthermore, we also observed that halofuginone treatment blocked the T-helper 17 (Th17) cell differentiation in vivo and in vitro. We demonstrated for the first time that halofuginone alleviated the onset of periodontitis through reducing immune responses.
AuthorsJiang Wang, Bo Wang, Xin Lv, Yingjie Wang
JournalInternational journal of immunopathology and pharmacology (Int J Immunopathol Pharmacol) 2020 Jan-Dec Vol. 34 Pg. 2058738420974893 ISSN: 2058-7384 [Electronic] England
PMID33259259 (Publication Type: Journal Article)
Chemical References
  • Cytokines
  • Immunologic Factors
  • Inflammation Mediators
  • Piperidines
  • Quinazolinones
  • halofuginone
Topics
  • Animals
  • Bacteroidaceae Infections (drug therapy, immunology, metabolism, microbiology)
  • Cell Differentiation (drug effects)
  • Cells, Cultured
  • Chronic Periodontitis (drug therapy, immunology, metabolism, microbiology)
  • Cytokines (metabolism)
  • Disease Models, Animal
  • Gingiva (drug effects, immunology, metabolism, microbiology)
  • Host-Pathogen Interactions
  • Immunologic Factors (pharmacology)
  • Inflammation Mediators (metabolism)
  • Mice, Inbred C57BL
  • Piperidines (pharmacology)
  • Porphyromonas gingivalis (immunology)
  • Quinazolinones (pharmacology)
  • Th17 Cells (drug effects, immunology, metabolism)

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