Gut microbiota contributes to the development of hypertension in a genetic mouse model of systemic lupus erythematosus.

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Hypertension is an important cardiovascular risk factor that is prevalent in the systemic lupus erythematosus (SLE) patient population. Here, we have investigated whether intestinal microbiota is involved in hypertension in a genetic mouse model of SLE.Twenty-six-week-old female NZW/LacJ (control) and NZBWF1 (F1 hybrid of New Zealand Black and New Zealand White strains) (SLE) mice were treated for 6 weeks with a broad-spectrum antibiotic mixture or with vancomycin. Faecal microbiota transplantation (FMT) was performed from donor SLE group to recipient to germ-depleted or germ-free mice.Antibiotic treatment inhibited the development of hypertension, renal injury, improved endothelial dysfunction and vascular oxidative stress, and decreased aortic helper T (Th)17 infiltration in NZBWF1 mice. High blood pressure (BP) and vascular complications found in SLE mice, but not autoimmunity, kidney inflammation, and endotoxemia, were reproduced by the transfer of gut microbiota from SLE donors to germ-free or germ-depleted mice. Increased proportions of Bacteroides were linked with high BP in these mice. The reduced endothelium-dependent vasodilator responses to acetylcholine and the high BP induced by microbiota from hypertensive SLE mice were inhibited after interleukin-17 neutralization.Changes in T cell populations, endothelial function, vascular inflammation and hypertension driven by a genetic SLE background can be modified by antibiotic-induced changes in gut microbiota. The vascular changes induced by hypertensive SLE microbiota were mediated by Th17 infiltration in the vasculature.

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Authors: Néstor de la Visitación, Iñaki Robles-Vera, Marta Toral, Manuel Gómez-Guzmán, Manuel Sánchez, Javier Moleón, Cristina González-Correa, Natividad Martín-Morales, Francisco O’Valle, Rosario Jiménez, Miguel Romero, Juan Duarte