Intestinal dysbiosis in systemic lupus erythematosus: cause or consequence?

López, Patricia; Sánchez, Borja; Margollés, Abelardo

doi:10.1097/bor.0000000000000309

Cited by 45 publications

(36 citation statements)

References 63 publications

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“…In patients with SLE, a lower Firmicutes / Bacteroidetes ratio and the abundance of several genera have been reported: Rhodococcus , Eggerthella , Klebsiella , Prevotella , Eubacterium and Flavonifractor were enriched significantly, while Dialister and Pseudobutyrivibrio were decreased in SLE patients . It is not known whether the alteration of commensal bacteria results as a consequence of the disease process or dysbiosis contributes to the lupus onset . According to Johnson et al .…”

Section: Systemic Lupus Erythematosus (Sle)mentioning

confidence: 99%

“…However, in previous years it has been suggested, as in other autoimmune diseases, that the gut microbiota could play an important role in the development of SLE ( [74,75]. It is not known whether the alteration of commensal bacteria results as a consequence of the disease process or dysbiosis contributes to the lupus onset [76]. According to Johnson et al [77], dysbiosis is associated with local inflammatory responses (specifically the Th17 response) and high circulating levels of antibodies against ds-DNA and histone.…”

Section: Systemic Lupus Erythematosus (Sle)mentioning

confidence: 99%

mentioning

confidence: 99%

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The microbiome in autoimmune diseases

Luca

Shoenfeld

2018

Clinical and Experimental Immunology

369

241

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SummaryThe microbiome is represented by microorganisms which live in a symbiotic way with the mammalian. Microorganisms have the ability to influence different physiological aspects such as the immune system, metabolism and behaviour. In recent years, several studies have highlighted the role of the microbiome in the pathogenesis of autoimmune diseases. Notably, in systemic lupus erythematosus an alteration of the intestinal flora (lower Firmicutes/Bacteroidetes ratio) has been described. Conversely, changes to the gut commensal and periodontal disease have been proposed as important factors in the pathogenesis of rheumatoid arthritis. At the same time, other autoimmune diseases (i.e. systemic sclerosis, Sjögren's syndrome and anti-phospholipid syndrome) also share modifications of the microbiome in the intestinal tract and oral flora. Herein, we describe the role of the microbiome in the maintenance homeostasis of the immune system and then the alterations of the microorganisms that occur in systemic autoimmune diseases. Finally, we will consider the use of probiotics and faecal transplantation as novel therapeutic targets.

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Section: Systemic Lupus Erythematosus (Sle)mentioning

confidence: 99%

Section: Systemic Lupus Erythematosus (Sle)mentioning

confidence: 99%

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The microbiome in autoimmune diseases

Luca

Shoenfeld

2018

Clinical and Experimental Immunology

369

241

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“…Gut microbiota might trigger symptoms and progression of some autoimmune diseases (6). A disbalance in gut microbiota populations in SLE patients was described, characterized by a significantly lower Firmicutes/ Bacteroidetes (F/B) ratio (6,7), a lower diversity of gut microbiota, and changes in several bacterial species, in particular, an increased representation of Gram-negative bacteria consistent with an increased serum level of LPS (8). In lupus-prone Murphy Roths Large (MLR)/Mp-Faslpr (lpr) mice, it has been described that the dynamics of microbiota play a critical role in lupus pathogenesis (9).…”

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confidence: 99%

Lactobacillus fermentum CECT5716: a novel alternative for the prevention of vascular disorders in a mouse model of systemic lupus erythematosus

et al. 2019

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The aim of the present study was to examine whether the immune‐modulatory bacteria Lactobacillus fermentum CECT5716 (LC40) ameliorates disease activity and cardiovascular complications in a female mouse model of lupus. Eighteen‐week‐old NZBWF1 [systemic lupus erythematosus (SLE)] and NZW/LacJ (control) mice were treated with vehicle or LC40 (5 × 108 colony‐forming units/d) for 15 wk. LC40 treatment reduced lupus disease activity, blood pressure, cardiac and renal hypertrophy, and splenomegaly in SLE mice. LC40 reduced the elevated T, B, regulatory T cells (Treg), and T helper (Th)‐1 cells in mesenteric lymph nodes of lupus mice. LC40 lowered the higher plasma concentration of proinflammatory cytokines observed in lupus mice. Aortas from SLE mice showed reduced endothelium‐dependent vasodilator responses to acetylcholine. Endothelial dysfunction found in SLE is related to an increase of both NADPH oxidase‐driven superoxide production and eNOS phosphorylation at the inhibitory Thr495. These activities returned to normal values after a treatment with LC40. Probiotic administration to SLE mice reduced plasma LPS levels, which might be related to an improvement of the gut barrier integrity. LC40 treatment increases the Bifidobacterium count in gut microbiota of SLE mice. In conclusion, our findings identify the gut microbiota manipulation with LC40 as an alternative approach to the prevention of SLE and its associated vascular damage.—Toral, M., Robles‐Vera, I., Romero, M., de la Visitación, N., Sánchez, M., O'Valle, F., Rodriguez‐Nogales, A., Gálvez, J., Duarte, J., Jiménez, R. Lactobacillus fermentum CECT5716: a novel alternative for the prevention of vascular disorders in a mouse model of systemic lupus erythematosus. FASEB J. 33, 10005–10018 (2019). http://www.fasebj.org

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“…Changes in intestinal microbiome have been found both in lupus animal models and in SLE patients, however the exact cause-effect relationship between alterations of the gut bacterial composition and the development of the disease remains still to be elucidated. Two different models of interaction between the gut microbiome and the immune system in SLE have been proposed [49]. In the first, it has been hypothesized that, in a pre-clinical stage of SLE, dysbiosis could promote an aberrant mucosal immune response to self-antigens, and as a consequence, enhance a local and systemic inflammatory state with hyperactive antibody production and disease manifestations in predisposed subjects.…”

Section: Systemic Lupus Erythematosusmentioning

confidence: 99%

The role of the gastrointestinal tract in the pathogenesis of rheumatic diseases

Ciccia

Ferrante

Guggino

et al. 2016

Best Practice & Research Clinical Rheumatology

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a b s t r a c tDysregulation of the intestinal epithelial barrier in genetically susceptible individuals may lead to both intestinal and extraintestinal autoimmune disorders. There is emerging literature on the role of microbiota changes in the pathogenesis of systemic rheumatic diseases such as rheumatoid arthritis, spondyloarthropathies, and connective tissue diseases. Although the role of the gastrointestinal tract in the pathogenesis of spondyloartropathies is well defined and many studies underline the importance of gastrointestinal inflammation in modulating local and systemic inflammation, the data are inconclusive regarding the effect of dysbiosis on rheumatoid arthritis and connective tissue diseases. This review aims to summarize current data on the role of the gastrointestinal involvement and intestinal microbiota in the pathogenesis of systemic rheumatic disease.

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Intestinal dysbiosis in systemic lupus erythematosus: cause or consequence?

Abstract: Recent findings support an important role for the crosstalk between bacteria and immune cells to maintain an intestinal homeostasis crucial to sustain tolerance toward self-antigens and intestinal microbiota.

Cited by 45 publications

References 63 publications

The microbiome in autoimmune diseases

The microbiome in autoimmune diseases

Lactobacillus fermentum CECT5716: a novel alternative for the prevention of vascular disorders in a mouse model of systemic lupus erythematosus

The role of the gastrointestinal tract in the pathogenesis of rheumatic diseases

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