Gut microbiota and rheumatoid arthritis: From pathogenesis to novel therapeutic opportunities

Zhao, Ting; Wang, Yuanyuan; Zhu, Youyang; Xie, Zhaohu; Hai, Qingshan; Li, Zhaofu; Qin, Dongdong

doi:10.3389/fimmu.2022.1007165

Cited by 85 publications

(76 citation statements)

References 85 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The disruption of the epithelial barrier function occurs in the preclinical phase of RA in murine models and humans (Tajik et al, 2020;Audo et al, 2022). Gut dysbiosis might trigger the breakdown of gut barrier integrity and the leakage of microbiota or their metabolites into gut tissue and even venous or lymphatic circulation, enabling exposure of the immune cells to bacterial antigens leading to local and systemic inflammation, increased pro-inflammatory cytokines such as TNF-a and IL-17A, and differentiation of autoreactive Th17 cells (Figure 2) (Berthelot et al, 2019;Chiang et al, 2019;Man et al, 2020;Tajik et al, 2020;Garabatos and Santamaria, 2022;Zhao et al, 2022). The migration of self-reactive cells to the joints can cause cartilage and bone damage (Zhao et al, 2022).…”

Section: Alterations In Gut Barrier Functionmentioning

confidence: 99%

“…These cytokines lead to synovial hyperplasia, pannus formation, and destruction of cartilage and joints. Pro-inflammatory cytokines induce fibroblasts to produce matrix metalloproteinases and RANKL (receptor activator of nuclear factor kB ligand), which mediate the destruction of bone and cartilage tissue, leading to the development of RA (Zhao et al, 2022).…”

Section: Gut Dysbiosis Induces the Development Of Chronic Inflammatio...mentioning

confidence: 99%

“…Bacterial strains from the human intestine can regulate the differentiation and activation of Th17 and Treg cells (Narushima et al, 2014). Intestinal mucosa contains many Th17 and Treg cells (Zhao et al, 2022). Th17 cells usually are in the gut in a microbiotadependent manner, maintaining tissue homeostasis and fighting against extracellular bacteria and fungi.…”

Section: Gut Microbiota Can Modulate the Th17/treg Balancementioning

confidence: 99%

See 2 more Smart Citations

Gut-joint axis: Gut dysbiosis can contribute to the onset of rheumatoid arthritis via multiple pathways

Romero-Figueroa

Ramírez-Durán²,

Montiel-Jarquín³

et al. 2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

Rheumatoid Arthritis (RA) is an autoimmune disease characterized by loss of immune tolerance and chronic inflammation. It is pathogenesis complex and includes interaction between genetic and environmental factors. Current evidence supports the hypothesis that gut dysbiosis may play the role of environmental triggers of arthritis in animals and humans. Progress in the understanding of the gut microbiome and RA. has been remarkable in the last decade. In vitro and in vivo experiments revealed that gut dysbiosis could shape the immune system and cause persistent immune inflammatory responses. Furthermore, gut dysbiosis could induce alterations in intestinal permeability, which have been found to predate arthritis onset. In contrast, metabolites derived from the intestinal microbiota have an immunomodulatory and anti-inflammatory effect. However, the precise underlying mechanisms by which gut dysbiosis induces the development of arthritis remain elusive. This review aimed to highlight the mechanisms by which gut dysbiosis could contribute to the pathogenesis of RA. The overall data showed that gut dysbiosis could contribute to RA pathogenesis by multiple pathways, including alterations in gut barrier function, molecular mimicry, gut dysbiosis influences the activation and the differentiation of innate and acquired immune cells, cross-talk between gut microbiota-derived metabolites and immune cells, and alterations in the microenvironment. The relative weight of each of these mechanisms in RA pathogenesis remains uncertain. Recent studies showed a substantial role for gut microbiota-derived metabolites pathway, especially butyrate, in the RA pathogenesis.

show abstract

Section: Alterations In Gut Barrier Functionmentioning

confidence: 99%

Section: Gut Dysbiosis Induces the Development Of Chronic Inflammatio...mentioning

confidence: 99%

Section: Gut Microbiota Can Modulate the Th17/treg Balancementioning

confidence: 99%

See 1 more Smart Citation

Gut-joint axis: Gut dysbiosis can contribute to the onset of rheumatoid arthritis via multiple pathways

Romero-Figueroa

Ramírez-Durán²,

Montiel-Jarquín³

et al. 2023

Front. Cell. Infect. Microbiol.

View full text Add to dashboard Cite

show abstract

“…At present, the mechanisms of GM participating in RA pathogenesis mainly include regulating the differentiation of immune cells, inducing the production of inflammatory mediators, and molecular simulation. Disturbed GM can trigger the innate and adaptive immunity abnormally, which may lead to aberrant systemic immunity (55)(56)(57). The mucosal immunity is the first line of defense against exogenous pathogens in the gastrointestinal tract (58,59).…”

Section: Relationship Between Ra and Gmmentioning

confidence: 99%

Relationship between gut microbiota and rheumatoid arthritis: A bibliometric analysis

Dong

Yao²,

Deng³

et al. 2023

Front. Immunol.

View full text Add to dashboard Cite

IntroductionRheumatoid arthritis (RA) is a multifactorial autoimmune disease. Recently, growing evidence demonstrates that gut microbiota (GM) plays an important role in RA. But so far, no bibliometric studies pertaining to GM in RA have ever been published. This study attempts to depict the knowledge framework in this field from a holistic and systematic perspective based on the bibliometric analysis.MethodsLiterature related to the involvement of GM in RA was searched and picked from the Web of Science Core Collection (WOSCC) database. The annual output, cooperation, hotspots, research status and development trend of this field were analyzed by bibliometric software (VOSviewer and Bibliometricx).Results255 original research articles and 204 reviews were included in the analysis. The articles in this field that can be retrieved in WOSCC were first published in 2004 and increased year by year since then. 2013 is a growth explosion point. China and the United States are the countries with the most contributions, and Harvard University is the affiliation with the most output. Frontiers in Immunology (total citations = 603) is the journal with the most publications and the fastest growth rate. eLife is the journal with the most citations (total citations = 1248). Scher, Jose U. and Taneja, Veena are the most productive and cited authors. The research in this field is mainly distributed in the evidence, mechanism and practical application of GM participating in RA through the analysis of keywords and documents. There is sufficient evidence to prove the close relationship between GM and RA, which lays the foundation for this field. This extended two colorful and tender branches of mechanism research and application exploration, which have made some achievements but still have broad exploration space. Recently, the keywords ”metabolites“, ”metabolomics“, ”acid“, ”b cells“, ”balance“, ”treg cells“, ”probiotic supplementation“ appeared most frequently, which tells us that research on the mechanism of GM participating in RA and exploration of its application are the hotspots in recent years.DiscussionTaken together, these results provide a data-based and objective introduction to the GM participating in RA, giving readers a valuable reference to help guide future research.

show abstract

“…Drugs used for the treatment of CTDs and vasculitis can also affect the gut microbiota. Methotrexate, sulfasalazine, etanercept and tocilizumab for example have been shown to restore normal microbiota in patients with RA [ 78 ]. Pharmacomicrobiomic studies can help understand the role of the gut microbiome in the various efficacy of anti-rheumatic drugs in patients with autoimmune diseases [ 72 ].…”

Section: Potential Microbiome Therapeutics For Ctd-ild and Vasculitismentioning

confidence: 99%

The Role of the Microbiome in Connective-Tissue-Associated Interstitial Lung Disease and Pulmonary Vasculitis

et al. 2022

View full text Add to dashboard Cite

The microbiome can trigger and maintain immune-mediated diseases and is associated with the severity and prognosis of idiopathic pulmonary fibrosis, which is the prototype of interstitial lung diseases (ILDs). The latter can be a major cause of morbidity and mortality in patients with connective-tissue diseases (CTD). In the present review, we discuss the current evidence regarding microbiome in CTD-ILD and pulmonary vasculitis. In patients with rheumatoid arthritis (RA) the BAL microbiota is significantly less diverse and abundant, compared to healthy controls. These changes are associated with disease severity. In systemic sclerosis (SSc), gastrointestinal (GI)-dysbiosis is associated with ILD. Butyrate acid administration as a means of restoration of GI-microbiota has reduced the degree of lung fibrosis in animal models. Although related studies are scarce for SLE and Sjögren’s syndrome, studies of the gut, oral and ocular microbiome provide insights into the pathogenesis of these diseases. In ANCA-associated vasculitis, disease severity and relapses have been associated with disturbed nasal mucosa microbiota, with immunosuppressive treatment restoring the microbiome changes. The results of these studies suggest however no causal relation. More studies of the lung microbiome in CTD-ILDs are urgently needed, to provide a better understanding of the pathogenesis of these diseases.

show abstract

Gut microbiota and rheumatoid arthritis: From pathogenesis to novel therapeutic opportunities

Cited by 85 publications

References 85 publications

Gut-joint axis: Gut dysbiosis can contribute to the onset of rheumatoid arthritis via multiple pathways

Gut-joint axis: Gut dysbiosis can contribute to the onset of rheumatoid arthritis via multiple pathways

Relationship between gut microbiota and rheumatoid arthritis: A bibliometric analysis

The Role of the Microbiome in Connective-Tissue-Associated Interstitial Lung Disease and Pulmonary Vasculitis

Contact Info

Product

Resources

About