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Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model

OBJECTIVES: This study intended to explore the effect of T regulatory cells (Tregs) in the perinatal liver against LPS-induced inflammation in a preterm birth mouse model. Moreover, the role of adoptive Tregs on the inflammatory response induced by LPS was also studied. METHODS: Female BALB/C mice w...

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Autores principales: Siddiq, Muhammad, Wang, Fan, Xiao, Mi, Lin, Xiao Jie, Fatima, Nazira, Iqbal, Sara, Iqbal, Umar, Piao, Xian-Hua, Liu, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Faculdade de Medicina / USP 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7603294/
https://www.ncbi.nlm.nih.gov/pubmed/33206750
http://dx.doi.org/10.6061/clinics/2020/e1665
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author Siddiq, Muhammad
Wang, Fan
Xiao, Mi
Lin, Xiao Jie
Fatima, Nazira
Iqbal, Sara
Iqbal, Umar
Piao, Xian-Hua
Liu, Li
author_facet Siddiq, Muhammad
Wang, Fan
Xiao, Mi
Lin, Xiao Jie
Fatima, Nazira
Iqbal, Sara
Iqbal, Umar
Piao, Xian-Hua
Liu, Li
author_sort Siddiq, Muhammad
collection PubMed
description OBJECTIVES: This study intended to explore the effect of T regulatory cells (Tregs) in the perinatal liver against LPS-induced inflammation in a preterm birth mouse model. Moreover, the role of adoptive Tregs on the inflammatory response induced by LPS was also studied. METHODS: Female BALB/C mice were injected intraperitoneally (IP) with LPS dissolved in normal saline solution at a dose of 50 µg/kg. Spleens from pregnant mice were used to obtain Tregs. The expression of Forkhead family transcription factor-3 (Foxp3), Interleukin-6 (IL-6), Toll-like receptor-4 (TLR-4), and Heme oxygenase-1 (HO-1) were assessed from fetal liver tissues by polymerase chain reaction and western blotting. RESULTS: LPS administered to mice induced an inflammatory response in the perinatal liver, and this inflammatory response was negatively regulated by Tregs in the experimental group. Maternal-fetal tolerance was maintained by Tregs. Transmission of Tregs was estimated in different experimental groups based on the mRNA expression of TLR-4, IL-6, HO-1, and Foxp3. CONCLUSIONS: After analysis of the experimental data, it was determined that Tregs exhibited regulatory potential against LPS-induced inflammatory response. Further, it was concluded that the transmission of Tregs improved the mother’s immune tolerance against LPS-induced inflammation in the fetal liver.
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spelling pubmed-76032942020-11-10 Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model Siddiq, Muhammad Wang, Fan Xiao, Mi Lin, Xiao Jie Fatima, Nazira Iqbal, Sara Iqbal, Umar Piao, Xian-Hua Liu, Li Clinics (Sao Paulo) Original Article OBJECTIVES: This study intended to explore the effect of T regulatory cells (Tregs) in the perinatal liver against LPS-induced inflammation in a preterm birth mouse model. Moreover, the role of adoptive Tregs on the inflammatory response induced by LPS was also studied. METHODS: Female BALB/C mice were injected intraperitoneally (IP) with LPS dissolved in normal saline solution at a dose of 50 µg/kg. Spleens from pregnant mice were used to obtain Tregs. The expression of Forkhead family transcription factor-3 (Foxp3), Interleukin-6 (IL-6), Toll-like receptor-4 (TLR-4), and Heme oxygenase-1 (HO-1) were assessed from fetal liver tissues by polymerase chain reaction and western blotting. RESULTS: LPS administered to mice induced an inflammatory response in the perinatal liver, and this inflammatory response was negatively regulated by Tregs in the experimental group. Maternal-fetal tolerance was maintained by Tregs. Transmission of Tregs was estimated in different experimental groups based on the mRNA expression of TLR-4, IL-6, HO-1, and Foxp3. CONCLUSIONS: After analysis of the experimental data, it was determined that Tregs exhibited regulatory potential against LPS-induced inflammatory response. Further, it was concluded that the transmission of Tregs improved the mother’s immune tolerance against LPS-induced inflammation in the fetal liver. Faculdade de Medicina / USP 2020-11-02 2020 /pmc/articles/PMC7603294/ /pubmed/33206750 http://dx.doi.org/10.6061/clinics/2020/e1665 Text en Copyright © 2020 CLINICS http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons License (http://creativecommons.org/licenses/by/4.0/) which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is properly cited.
spellingShingle Original Article
Siddiq, Muhammad
Wang, Fan
Xiao, Mi
Lin, Xiao Jie
Fatima, Nazira
Iqbal, Sara
Iqbal, Umar
Piao, Xian-Hua
Liu, Li
Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
title Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
title_full Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
title_fullStr Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
title_full_unstemmed Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
title_short Inhibition of lipopolysaccharide-induced inflammation via the protective role of T regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
title_sort inhibition of lipopolysaccharide-induced inflammation via the protective role of t regulatory cells in the fetal liver in a late-pregnancy preterm mouse model
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7603294/
https://www.ncbi.nlm.nih.gov/pubmed/33206750
http://dx.doi.org/10.6061/clinics/2020/e1665
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