Probiotics Prevent Hypertension in a Murine Model of Systemic Lupus Erythematosus Induced by Toll-Like Receptor 7 Activation
Metadatos
Mostrar el registro completo del ítemAutor
de la Visitación, Néstor; Robles Vera, Iñaki; Moleón Moya, Javier; Sánchez Santos, Manuel; Jiménez Moleón, Rosario; Gómez Guzmán, Manuel; González Correa, Cristina; Olivares, Mónica; Romero Pérez, Miguel; Duarte Pérez, Juan ManuelEditorial
MDPI
Materia
Probiotics Hypertension Endothelial dysfunction TLR7 activation Lupus
Fecha
2021-07-31Referencia bibliográfica
de la Visitación, N... [et al.]. Probiotics Prevent Hypertension in a Murine Model of Systemic Lupus Erythematosus Induced by Toll-Like Receptor 7 Activation. Nutrients 2021, 13, 2669. [https://doi.org/10.3390/nu13082669]
Patrocinador
Comision Interministerial de Ciencia y Tecnologia, Ministerio de Economia y competitividad SAF2017-84894-R; Junta de Andalucia CTS-164; European Commission; Ministerio de Economia y Competitividad, Instituto de Salud Carlos III (CIBER-CV; Ciberes), Spain; European Union (Fondo Europeo de Desarrollo Regional, FEDER, "FEDER una manera de hacer Europa")Resumen
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
-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.