Galectin-3 Plays an Important Role in Preterm Birth Caused by Dental Infection of Porphyromonas Gingivalis

Sci Rep. 2018 Feb 12;8(1):2867. doi: 10.1038/s41598-018-21072-y.


Dental infection is risk for preterm birth (PTB) through unclear mechanisms. We established a dental infection-induced PTB mouse model, in which Porphyromonas gingivalis (P.g.) induced PTB by 2 days. We analysed pathogenic factors contributing to PTB and their effects on trophoblasts in vitro. TNF-α, IL-8, and COX-2 were upregulated in P.g.-infected placenta. Galectin-3 (Gal-3), an immune regulator, was significantly upregulated in placenta, amniotic fluid, and serum. In vitro, P.g.-lipopolysaccharide (P.g.-LPS) increased TNF-α and Gal-3 in trophoblasts via NF-κB/MAPK signalling. Gal-3 inhibition significantly downregulated P.g.-LPS-induced TNF-α production. TNF-α upregulated Gal-3. Gal-3 also increased cytokines and Gal-3 through NF-κB/MAPK signalling. Moreover, Gal-3 suppressed CD-66a expression at the maternal-foetal interface. Co-stimulation with Gal-3 and P.g.-LPS upregulated cytokine levels, while Gal-3 plus Aggregatibacter actinomycetemcomitans (A.a.)- or Escherichia coli (E. coli)-LPS treatment downregulated them, indicating the critical role of Gal-3 especially in P.g. dental infection-induced PTB. P.g.-dental infection induced PTB, which was associated with Gal-3-dependent cytokine production. New therapies and/or diagnostic systems targeting Gal-3 may reduce PTB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amniotic Fluid / metabolism
  • Animals
  • Bacteroidaceae Infections / complications*
  • Cell Line
  • Disease Models, Animal
  • Female
  • Galectin 3 / blood
  • Galectin 3 / metabolism*
  • Humans
  • Lipopolysaccharides / adverse effects
  • MAP Kinase Signaling System / drug effects
  • Maternal Exposure / adverse effects*
  • Mice
  • Placenta / metabolism
  • Porphyromonas gingivalis / metabolism*
  • Pregnancy
  • Premature Birth / microbiology*
  • Trophoblasts / cytology
  • Trophoblasts / drug effects
  • Trophoblasts / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Up-Regulation*


  • Galectin 3
  • Lipopolysaccharides
  • Tnf protein, mouse
  • Tumor Necrosis Factor-alpha
  • galectin-3, human