Synthetic Bacterial Consortia Transplantation Attenuates Vaginal Inflammation and Modulates the Immune Response in a Mouse Model of Gardnerella vaginalis-Induced Bacterial Vaginosis

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The study evaluated synthetic bacterial consortia transplantation (SBCT) versus vaginal microbiota transplantation (VMT) and saline in a mouse model of Gardnerella vaginalis-induced bacterial vaginosis, assessing histopathology, inflammatory cytokines, pro-inflammatory biomarkers, helper T-cell transcription factors, NF-κB activity, and vaginal microbiota composition. SBCT and VMT both suppressed G. vaginalis growth, reduced epithelial damage and inflammation, decreased pro-inflammatory IL-1β and IL-8, increased IL-10, inhibited NF-κB activation, suppressed IL-17, and enhanced Foxp3 expression while restoring vaginal microbiota diversity. A major caveat explicitly indicated by the publication status is that this work is a preprint and has not been peer reviewed. The paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract Bacterial vaginosis (BV) disrupts the vaginal microbiota, leading to health risks. Antibiotics often fail to prevent recurrence. This study examines synthetic bacterial consortia transplantation (SBCT) as a safer, more controlled treatment alternative to restore healthy vaginal flora and immune response, showing promise against BV. This study aimed to evaluate the efficacy of SBCT and compare it with VMT in a mouse model of Gardnerella vaginalis-induced BV. A murine model of G. vaginalis-induced BV was established, and mice were treated with SBCT, VMT, or saline. Histopathological changes, inflammatory cytokine levels, pro-inflammatory biomarker expression, helper T cell transcription factor expression, and vaginal microbiota composition were assessed. SBCT and VMT effectively suppressed G. vaginalis growth, reduced inflammation, and restored vaginal microbiota diversity. Both treatments attenuated epithelial damage, downregulated pro-inflammatory cytokines (IL-1β and IL-8), and upregulated the anti-inflammatory cytokine IL-10. SBCT and VMT also inhibited NF-κB activation, suppressed IL-17 expression, and enhanced Foxp3 expression in vaginal tissues. SBCT is a promising therapeutic approach for treating BV, as it effectively modulates the immune response and restores vaginal microbiota diversity in a mouse model of G. vaginalis-induced BV.
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Synthetic Bacterial Consortia Transplantation Attenuates Vaginal Inflammation and Modulates the Immune Response in a Mouse Model of Gardnerella vaginalis-Induced Bacterial Vaginosis | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Synthetic Bacterial Consortia Transplantation Attenuates Vaginal Inflammation and Modulates the Immune Response in a Mouse Model of Gardnerella vaginalis-Induced Bacterial Vaginosis Ying Liu, Liang He, Yan Hu, Xingya Liao, Hongyan Wang, Linlin Yang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4562682/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 3 You are reading this latest preprint version Abstract Bacterial vaginosis (BV) disrupts the vaginal microbiota, leading to health risks. Antibiotics often fail to prevent recurrence. This study examines synthetic bacterial consortia transplantation (SBCT) as a safer, more controlled treatment alternative to restore healthy vaginal flora and immune response, showing promise against BV. This study aimed to evaluate the efficacy of SBCT and compare it with VMT in a mouse model of Gardnerella vaginalis-induced BV. A murine model of G. vaginalis-induced BV was established, and mice were treated with SBCT, VMT, or saline. Histopathological changes, inflammatory cytokine levels, pro-inflammatory biomarker expression, helper T cell transcription factor expression, and vaginal microbiota composition were assessed. SBCT and VMT effectively suppressed G. vaginalis growth, reduced inflammation, and restored vaginal microbiota diversity. Both treatments attenuated epithelial damage, downregulated pro-inflammatory cytokines (IL-1β and IL-8), and upregulated the anti-inflammatory cytokine IL-10. SBCT and VMT also inhibited NF-κB activation, suppressed IL-17 expression, and enhanced Foxp3 expression in vaginal tissues. SBCT is a promising therapeutic approach for treating BV, as it effectively modulates the immune response and restores vaginal microbiota diversity in a mouse model of G. vaginalis-induced BV. Bacterial vaginosis Gardnerella vaginalis synthetic bacterial consortia transplantation vaginal microbiota transplantation inflammation immune response Full Text Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editor assigned by journal 11 Jun, 2024 Submission checks completed at journal 11 Jun, 2024 First submitted to journal 11 Jun, 2024 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. 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