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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.

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