ArticleScientific reports2018
Galectin-3 Plays an Important Role in Preterm Birth Caused by Dental Infection of Porphyromonas gingivalis.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Identification of cell senescence-related genes in spontaneous preterm birth based on bioinformatics analysis and machine learning.PloS one · 2026Article
- Heat stress-induced gut dysbiosis and multi-organ injury: mechanisms and therapeutic modulation.Frontiers in cellular and infection microbiology · 2026Review
- Clinical Periodontal Evaluation and Assessment of Dipeptidyl-Peptidase-4 and Galectin-3 in Gingival Crevicular Fluid of Periodontitis Patients with Heart Failure and Diabetes.Journal of clinical medicine · 2025Article
- Melatonin alleviates high temperature exposure induced fetal growth restriction via the gut-placenta-fetus axis in pregnant mice.Journal of advanced research · 2025Article
- Exploring the Genetic and Functional Diversity ofInternational journal of molecular sciences · 2025Article
- Identification of nanaomycin A and its analogs by a newly established screening method for functional inhibitors of the type IX secretion system in Porphyromonas gingivalis.The Journal of antibiotics · 2025Article
- Gingival crevicular fluid galectin-3 and interleukin-1 beta levels in stage 3 periodontitis with grade B and C.Clinical oral investigations · 2023Article
- Porphyromonas gingivalis-odontogenic infection is the potential risk for progression of nonalcoholic steatohepatitis-related neoplastic nodule formation.Scientific reports · 2023Article
- Spontaneous Preterm Birth: Elevated Galectin-3 and Telomere Shortening May Reflect a Common Pathway of Enhanced Inflammation and Senescence.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- A placenta-on-a-chip model to determine the regulation of FKBPL and galectin-3 in preeclampsia.Cellular and molecular life sciences : CMLS · 2023Article
- Mouse maternal odontogenic infection withFrontiers in pediatrics · 2023Article
- The Expression of IL-1β Correlates with the Expression of Galectin-3 in the Tissue at the Maternal-Fetal Interface during the Term and Preterm Labor.Journal of clinical medicine · 2022Article
- Galectins-1, -3 and -9 Are Present in Breast Milk and Have a Role in Early Life Development.Nutrients · 2022Article
- Galectins: Important Regulators in Normal and Pathologic Pregnancies.International journal of molecular sciences · 2022Review
- The RagA and RagB proteins of Porphyromonas gingivalis.Molecular oral microbiology · 2021Review
- Inherently and Conditionally Essential Protein Catabolism Genes of Porphyromonas gingivalis.Trends in microbiology · 2021Review
- Review
- Role of galectin-glycan circuits in reproduction: from healthy pregnancy to preterm birth (PTB).Seminars in immunopathology · 2020Review
- Salivary proteome signatures in the early and middle stages of human pregnancy with term birth outcome.Scientific reports · 2020Article
- Invasion of Human Retinal Pigment Epithelial Cells by Porphyromonas gingivalis leading to Vacuolar/Cytosolic localization and Autophagy dysfunction In-Vitro.Scientific reports · 2020Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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