Probiotics Prevent Hypertension in a Murine Model of Systemic Lupus Erythematosus Induced by Toll-Like Receptor 7 Activation

Our group tested the effects of Lactobacillus fermentum CECT5716 (LC40) and/or Bifidobacterium breve CECT7263 (BFM) in the prevention of gut dysbiosis, hypertension and endothelial dysfunction in a pharmacologically-induced model of systemic lupus erythematosus (SLE). We treated eight-week-old BALB/...

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Veröffentlicht in:Nutrients 2021-07, Vol.13 (8), p.2669
Hauptverfasser: de la Visitación, Néstor, Robles-Vera, Iñaki, Moleón-Moya, Javier, Sánchez, Manuel, Jiménez, Rosario, Gómez-Guzmán, Manuel, González-Correa, Cristina, Olivares, Mónica, Toral, Marta, Romero, Miguel, Duarte, Juan
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container_issue 8
container_start_page 2669
container_title Nutrients
container_volume 13
creator de la Visitación, Néstor
Robles-Vera, Iñaki
Moleón-Moya, Javier
Sánchez, Manuel
Jiménez, Rosario
Gómez-Guzmán, Manuel
González-Correa, Cristina
Olivares, Mónica
Toral, Marta
Romero, Miguel
Duarte, Juan
description Our group tested the effects of Lactobacillus fermentum CECT5716 (LC40) and/or Bifidobacterium breve CECT7263 (BFM) in the prevention of gut dysbiosis, hypertension and endothelial dysfunction in a pharmacologically-induced model of systemic lupus erythematosus (SLE). We treated eight-week-old BALB/cByJRj mice without (Ctrl) or with the agonist of TLR-7 Imiquimod (IMQ) for 8 weeks. Concomitantly, LC40 (109 CFU/mL) and BFM (109 CFU/mL) were administered through oral gavage once a day. IMQ induced intestinal dysbiosis consisting of a decrease in the α-diversity measured with Chao-richness and numbers of species. LC40 and BFM did not restore these parameters. The three-dimensional principal component analysis of bacterial taxa in stool samples presented perfect clustering between Ctrl and IMQ groups. Clusters corresponding to LC40 and BFM were more akin to IMQ. BFM and LC40 were detected colonizing the gut microbiota of mice treated respectively. LC40 and BFM decreased plasma double-stranded DNA autoantibodies, and B cells in spleen, which were increased in the IMQ group. Also, LC40 and BFM treatments activated TLR9, reduced T cells activation, and Th17 polarization in mesenteric lymph nodes. Aortae from IMQ mice displayed a decreased endothelium-dependent vasodilator response to acetylcholine linked to pro-inflammatory and pro-oxidative status, which were normalized by both BFM and LC40. In conclusion, we demonstrate for the first time that the chronic treatment with LC40 or BFM prevented hypertension and endothelial dysfunction in a mouse lupus model induced by TLR-7 activation.
doi_str_mv 10.3390/nu13082669
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We treated eight-week-old BALB/cByJRj mice without (Ctrl) or with the agonist of TLR-7 Imiquimod (IMQ) for 8 weeks. Concomitantly, LC40 (109 CFU/mL) and BFM (109 CFU/mL) were administered through oral gavage once a day. IMQ induced intestinal dysbiosis consisting of a decrease in the α-diversity measured with Chao-richness and numbers of species. LC40 and BFM did not restore these parameters. The three-dimensional principal component analysis of bacterial taxa in stool samples presented perfect clustering between Ctrl and IMQ groups. Clusters corresponding to LC40 and BFM were more akin to IMQ. BFM and LC40 were detected colonizing the gut microbiota of mice treated respectively. LC40 and BFM decreased plasma double-stranded DNA autoantibodies, and B cells in spleen, which were increased in the IMQ group. Also, LC40 and BFM treatments activated TLR9, reduced T cells activation, and Th17 polarization in mesenteric lymph nodes. Aortae from IMQ mice displayed a decreased endothelium-dependent vasodilator response to acetylcholine linked to pro-inflammatory and pro-oxidative status, which were normalized by both BFM and LC40. 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Aortae from IMQ mice displayed a decreased endothelium-dependent vasodilator response to acetylcholine linked to pro-inflammatory and pro-oxidative status, which were normalized by both BFM and LC40. 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subjects Acetylcholine
Analysis
Animal models
Autoantibodies
Autoimmunity
B cells
Blood pressure
Blood vessels
Cardiovascular disease
Cell activation
Chronic conditions
Clustering
Coronary vessels
Deoxyribonucleic acid
Digestive system
Dilatation
DNA
Dysbacteriosis
Endothelium
Enzymes
Helper cells
Hypertension
Imiquimod
Inflammation
Intestinal microflora
Kidneys
Laboratory animals
Lupus
Lymph nodes
Lymphocytes
Lymphocytes B
Lymphocytes T
Microbiota
Microbiota (Symbiotic organisms)
Pathogens
Physiology
Plasma
Principal components analysis
Probiotics
Spleen
Systemic lupus erythematosus
T cells
Three dimensional analysis
TLR9 protein
Toll-like receptors
title Probiotics Prevent Hypertension in a Murine Model of Systemic Lupus Erythematosus Induced by Toll-Like Receptor 7 Activation
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