Gut microbiota: a newly identified environmental factor in systemic lupus erythematosus

Yao, Kaijin; Xie, Yong; Wang, Jiali; Lin, Yongda; Chen, Xiutian; Zhou, Tian-Biao

doi:10.3389/fimmu.2023.1202850

Cited by 7 publications

(3 citation statements)

References 110 publications

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“…The gut microbiota is increasingly recognized as a critical player in the development and modulation of autoimmune diseases, including SLE ( 43 ) and graft-versus-host disease, which shares some clinical signs as SLE ( 44 , 45 ). Our observation of distinct differences in the fecal microbiota diversity among Tlr5- deficient, heterozygous, and wild-type MRL/ lpr mice underscores a role of TLR5 in shaping the gut microbiota.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: Tlr5 deficiency exacerbates lupus-like disease in the MRL/lpr mouse model

Alajoleen,

Oakland,

Estaleen

et al. 2024

Front. Immunol.

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IntroductionLeaky gut has been linked to autoimmune disorders including lupus. We previously reported upregulation of anti-flagellin antibodies in the blood of lupus patients and lupus-prone mice, which led to our hypothesis that a leaky gut drives lupus through bacterial flagellin-mediated activation of toll-like receptor 5 (TLR5).MethodsWe created MRL/lpr mice with global Tlr5 deletion through CRISPR/Cas9 and investigated lupus-like disease in these mice.ResultContrary to our hypothesis that the deletion of Tlr5 would attenuate lupus, our results showed exacerbation of lupus with Tlr5 deficiency in female MRL/lpr mice. Remarkably higher levels of proteinuria were observed in Tlr5-/- MRL/lpr mice suggesting aggravated glomerulonephritis. Histopathological analysis confirmed this result, and Tlr5 deletion significantly increased the deposition of IgG and complement C3 in the glomeruli. In addition, Tlr5 deficiency significantly increased renal infiltration of Th17 and activated cDC1 cells. Splenomegaly and lymphadenopathy were also aggravated in Tlr5-/- MRL/lpr mice suggesting impact on lymphoproliferation. In the spleen, significant decreased frequencies of regulatory lymphocytes and increased germinal centers were observed with Tlr5 deletion. Notably, Tlr5 deficiency did not change host metabolism or the existing leaky gut; however, it significantly reshaped the fecal microbiota.ConclusionGlobal deletion of Tlr5 exacerbates lupus-like disease in MRL/lpr mice. Future studies will elucidate the underlying mechanisms by which Tlr5 deficiency modulates host-microbiota interactions to exacerbate lupus.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: Tlr5 deficiency exacerbates lupus-like disease in the MRL/lpr mouse model

Alajoleen,

Oakland,

Estaleen

et al. 2024

Front. Immunol.

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“…Novel approaches focused on the gut microbiome, including probiotics, prebiotics, and synbiotics, are emerging as promising methods to decelerate the advancement of inflammatory bowel diseases and promote intestinal health ( 60 ). The gut microbiota serves as a potential biomarker for the diagnosis and prognosis of systemic lupus erythematosus, and it also holds promise as a potential target for the treatment of systemic lupus erythematosus ( 61 ). Modulating the gut microbiota regulates distal symmetric polyneuropathy in diabetic patients ( 21 ).…”

Section: Discussionmentioning

confidence: 99%

Characteristics of gut microbiome in patients with pediatric solid tumor

Du,

Cui,

Fan

et al. 2024

Front. Pediatr.

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BackgroundPediatric solid tumors are a common malignant disease in children, and more and more studies have proved that there is an inseparable relationship between adult tumors and intestinal microbiome, but the changes in the intestinal microbiota of pediatric solid tumor (PST) patients have been scarcely examined. This study aims to examine the differences in the intestinal microbiota features between patients diagnosed with PST and healthy controls (HCs).MethodsTo elucidate the unique characteristics of the gut microbiota in pediatric patients with solid tumors, we recruited 23 PST patients and 20 HCs. A total of 43 stool samples were gathered, and then 16S rRNA sequencing was performed.ResultsWe noticed a noticeable pattern of elevated diversity in the gut microbiota within the PST groups. The differences in microbial communities among two groups were remarkable, regarding the analysis at the class level, the abundance of Bacilli was markedly increased in PST patients compared to HCs (P < 0.05), regarding the analysis at the genus level, The presence of Enterococcus was significantly higher in PST cases compared to HCs (P < 0.01), while Lachnospiraceae unclassified, Lachnospira, Haemophilus and Colidextribacter in PST cases, the abundance was significantly reduced. (P < 0.05), 6 genera, including Bacilli, Lactobacillales, Enterococcaceae and Morganella, showed a significant enrichment compared to healthy controls, while 10 genera, including Bilophila, Colidextribacter, Pasteurellales, Haemophilus, Lachnospiraceae unclassified, Lachnospira and Fusobacteriales, were significant reduction in the PST groups.ConclusionOur research conducted the characterization analysis of the gut microbiota in PST patients for the first time. More importantly, there are some notable differences in the gut microbiota between PST patients and healthy controls, which we believe is an interesting finding.

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“…Gut microbiota dysbiosis leads to both cytokines and immune cells dysregulation, contributing to the development and progression of SLE. Briefly, E. gallinarum and Ruminococcus are associated with an increase in Th17 cells and a reduction of Treg, with a Th17/Treg imbalance; E. gallinarum and L. reuteri increase the number of plasmacytoid dendritic cells and promote the production of IFN-I, one of the most important pathogenetic factors in SLE (110).…”

Section: Gut Microbiotamentioning

confidence: 99%

Environment and systemic lupus erythematosus

Cardelli,

Zucchi,

Elefante

et al. 2024

Clinical and Experimental Rheumatology

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a wide range of clinical manifestations and a relapsing-remitting course. SLE pathogenesis is the result of com plex interactions between ethnic, genetic, epigenetic, immunoregulatory, hor monal and environmental factors, and several aspects of these multifactori al connections are still unclear. Overall, for the disease development, an environmental trigger may induce immunological dysfunction in genetically predisposed individuals. This review aims to summarise the most relevant data on the impact of environmental factors on the incidence of SLE and on disease activity and damage in patients with an established diagnosis of SLE.

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Gut microbiota: a newly identified environmental factor in systemic lupus erythematosus

Cited by 7 publications

References 110 publications

RETRACTED: Tlr5 deficiency exacerbates lupus-like disease in the MRL/lpr mouse model

RETRACTED: Tlr5 deficiency exacerbates lupus-like disease in the MRL/lpr mouse model

Characteristics of gut microbiome in patients with pediatric solid tumor

Environment and systemic lupus erythematosus

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