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Shared Inflammatory Genetic Susceptibility Underlying Spontaneous Preterm Birth and Periodontitis

2025-09-02Artigo científico Acesso aberto
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dc.contributor.authorCouceiro, Joana
dc.contributor.authorFamilia, Carlos
dc.contributor.authorBrito, José
dc.contributor.authorMendes, José João
dc.contributor.authorBaptista, Pedro V.
dc.contributor.authorFernandes, Alexandra R.
dc.contributor.authorQuintas, Alexandre
dc.contributor.institutionUCIBIO - Applied Molecular Biosciences Unit
dc.contributor.institutionDCV - Departamento de Ciências da Vida
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2026-01-29T15:45:01Z
dc.date.available2026-01-29T15:45:01Z
dc.date.issued2025-09-02
dc.description.abstractBackground: Preterm birth (PTB) remains the leading cause of neonatal morbidity and mortality worldwide, with approximately two-thirds of cases occurring spontaneously (SPTB), but the etiology is still poorly understood. Chronic inflammatory diseases, such as periodontitis (PD), have been considered SPTB risk factors. However, we hypothesized that SPTB may instead represent a clinical manifestation of a broader genetic predisposition to dysregulated inflammation. Using PD as a model of chronic inflammation, we examined shared genetic susceptibility. Methods: In a case–control study (N = 126 Portuguese postpartum women), we screened 56 SNPs in 36 inflammation-related genes. Four functionally plausible variants (IL1RN rs4251961, TLR1 rs5743618, IL6 rs2069827, and IL6R rs4845617) were selected for detailed regression, adjusting for gestational age, floss usage, and an SPTBxPD interaction term. Results: IL1RN rs4251961 was recessively associated with SPTB risk, consistent with reduced IL-1RA expression linked to this variant. IL6R rs4845617 showed a modest protective effect. TLR1 rs5743618 exhibited the strongest association with the composite “inflammation” phenotype under multiple models, with CC homozygotes showing four-fold increased odds, independent of SPTB/PD co-occurrence. Conclusions: This study provides original evidence that shared genetic variants in inflammatory pathways—particularly TLR1 rs5743618—may underlie susceptibility to SPTB and PD. Our findings suggest a paradigm shift, viewing SPTB as a possible outcome of systemic inflammatory dysregulation rather than merely a consequence of comorbid inflammatory conditions. Future studies should validate this marker in larger cohorts.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent14
dc.format.extent279881
dc.identifier.doi10.3390/jcm14176195
dc.identifier.issn2077-0383
dc.identifier.otherPURE: 151504802
dc.identifier.otherPURE UUID: 8c8ba30b-a655-4a64-85d0-709ca7aa3d0b
dc.identifier.otherWOS: 001569839800001
dc.identifier.otherPubMed: 40943955
dc.identifier.otherScopus: 105016215780
dc.identifier.otherPubMedCentral: PMC12428887
dc.identifier.otherORCID: /0000-0001-5255-7095/work/204096497
dc.identifier.otherORCID: /0000-0003-2054-4438/work/204221187
dc.identifier.urihttp://hdl.handle.net/10362/199849
dc.identifier.urlhttps://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=nova_api&SrcAuth=WosAPI&KeyUT=WOS:001569839800001&DestLinkType=FullRecord&DestApp=WOS_CPL
dc.identifier.urlhttps://www.webofscience.com/wos/woscc/full-record/WOS:001569839800001
dc.language.isoeng
dc.peerreviewedyes
dc.subjectSpontaneous preterm birth
dc.subjectInflammation
dc.subjectPeriodontitis
dc.subjectGenetic polymorphism
dc.subjectTLR1
dc.subjectIL1RN
dc.subjectIL6
dc.subjectIL6R
dc.subjectCase–control study
dc.titleShared Inflammatory Genetic Susceptibility Underlying Spontaneous Preterm Birth and Periodontitisen
dc.title.subtitleA Case-Control Studyen
dc.typejournal article
degois.publication.firstPage1
degois.publication.issue17
degois.publication.lastPage14
degois.publication.titleJournal of Clinical Medicine
degois.publication.volume14
dspace.entity.typePublication
rcaap.rightsopenAccess

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