Resistant starch intake alleviates collagen-induced arthritis in mice by modulating gut microbiota and promoting concomitant propionate production

Bai, Yan; Li, Yanhong; Marion, Tony N.; Tong, Yanli; Zaiss, Mario M.; Tang, Zhigang; Zhang, Qiuping; Liu, Yi; Luo, Yubin

doi:10.1016/j.jaut.2020.102564

Cited by 61 publications

(60 citation statements)

References 57 publications

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“…The systemic administration of SCFAs was previously shown to reduce autoimmune disease by modulating T-cell-dependent autoimmunity [ 1 , 9 , 10 ]. To assess if propionate is also functional when administered locally, we used antigen-induced arthritis (AIA), a T-cell-dependent model of arthritis that relies on systemic immunization with methylated bovine serum albumin (mBSA) preceding local initiation of inflammation by intra-articular knee injection of mBSA [ 23 ].…”

Section: Resultsmentioning

confidence: 99%

“…In monocytes, SCFAs modulate production of inflammatory mediators, such as cytokines, chemokines, and prostaglandins [7] and in macrophages, butyrate reduced activity of the mechanistic Nutrients 2021, 13, 1643 2 of 11 target of rapamycin (mTOR) [8]. We and others have shown that SCFAs are also able to attenuate local joint inflammation and associated bone destruction in the preclinical T-cell-dependent collagen-induced arthritis (CIA) model [9,10]. In CIA, SCFAs exhibited effects on the adaptive T-cell response, especially by inducing Tregs, and both butyrate and PA directly changed the metabolism of osteoclast (OC) progenitors, thus effectively suppressing their differentiation into mature bone degrading OC [9,10].…”

Section: Introductionmentioning

confidence: 99%

“…We and others have shown that SCFAs are also able to attenuate local joint inflammation and associated bone destruction in the preclinical T-cell-dependent collagen-induced arthritis (CIA) model [ 9 , 10 ]. In CIA, SCFAs exhibited effects on the adaptive T-cell response, especially by inducing Tregs, and both butyrate and PA directly changed the metabolism of osteoclast (OC) progenitors, thus effectively suppressing their differentiation into mature bone degrading OC [ 9 , 10 ]. Accordingly, the gut microbiota is a strong regulator of systemic bone mass in mice, and SCFAs also regulated systemic bone mass in a noninflammatory model for postmenopausal bone loss [ 9 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

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Dietary Derived Propionate Regulates Pathogenic Fibroblast Function and Ameliorates Experimental Arthritis and Inflammatory Tissue Priming

et al. 2021

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Short-chain fatty acids are gut-bacteria-derived metabolites that execute important regulatory functions on adaptive immune responses, yet their influence on inflammation driven by innate immunity remains understudied. Here, we show that propionate treatment in drinking water or upon local application into the joint reduced experimental arthritis and lowered inflammatory tissue priming mediated by synovial fibroblasts. On a cellular level, incubation of synovial fibroblasts with propionate or a physiological mixture of short-chain fatty acids interfered with production of inflammatory mediators and migration and induced immune-regulatory fibroblast senescence. Our study suggests that propionate mediates its alleviating effect on arthritis by direct abrogation of local arthritogenic fibroblast function.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dietary Derived Propionate Regulates Pathogenic Fibroblast Function and Ameliorates Experimental Arthritis and Inflammatory Tissue Priming

et al. 2021

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“…SCFAs are produced by gut microbial fermentation of dietary fibre and include acetic acid, propionic acid and butyric acid, which provide nutrition for intestinal epithelial cells and inhibit the inflammatory response [51,52]. Specifically, Firmicutes produce high amounts of butyrate, whereas Bacteroidetes, including Bacteroides acidifaciens, produce high levels of acetate and propionate [53]. SCFAs regulate insulin-like growth factor-1 (IGF-1) and glucagon-like peptide-1 (GLP-1) via inhibition of histone deacetylase (HDAC) and activating receptor γ as a G-protein-coupled receptor ligand and peroxisome proliferator to indirectly promote bone formation as the signal molecules [36,54].…”

Section: Scfas May Promote Bone Homeostasismentioning

confidence: 99%

Bone Homeostasis and Gut Microbial-Dependent Signaling Pathways

Zhong

Zhang

Yin

et al. 2021

J. Microbiol. Biotechnol.

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Bone has self-healing and regenerative abilities and contains three types of cells in adults, including osteoblasts and osteocytes from mesenchymal stem cells and osteoclasts from haematopoietic cells in bone marrow. There are two key cell types that play an important role in bone homeostasis: osteoclasts that absorb bone matrix and osteoblasts that synthesise bone matrix. Osteocytes promote the balance of osteoblasts and osteoclasts in bone construction and bone remodeling, and maintain bone homeostasis by ensuring the balance of calcium and phosphorus metabolism [10]. Bone homeostasis is related to cell development and activation as well as mediation of metabolic and immune activities via signaling pathways. Recent research has shown that the BMP/SMADs, Wnt/β-catenin and OPG/RANKL/RANK signaling pathways play primary roles in bone homeostasis [11,12].Although research on the osteal signaling pathway has progressed, understanding of gut microbialdependent signaling pathways for metabolic and immune bone homeostasis remains elusive. In recent years, the study of gut microbiota has shed light on our understanding of bone homeostasis. Here, we review microbiota-mediated gut-bone crosstalk via bone morphogenetic protein/SMADs, Wnt and OPG/receptor activator of nuclear factor-kappa B ligand signaling pathways in direct (translocation) and indirect (metabolite) manners. The mechanisms underlying gut microbiota involvement in these signaling pathways are relevant in immune responses, secretion of hormones, fate of osteoblasts and osteoclasts and absorption of calcium. Collectively, we propose a signaling network for maintaining a dynamic homeostasis between the skeletal system and the gut ecosystem. Additionally, the role of gut microbial improvement by dietary intervention in osteal signaling pathways has also been elucidated. This review provides unique resources from the gut microbial perspective for the discovery of new strategies for further improving treatment of bone diseases by increasing the abundance of targeted gut microbiota.

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“…As previously described [25,26] , splenocytes and PBMCs from CIA mice were washed with PBS. For the analysis of Treg cells, cells were stained with anti-CD4-FITC (BD Bioscience), anti-CD25-PE-CY7 (BD Bioscience) and anti-Foxp3-PE (BD Bioscience).…”

Section: Intracellular Staining and Flow Cytometrymentioning

confidence: 99%

MicroRNA-143-3p alleviates murine collagen-induced arthritis by polarizing naive CD4+T cells into Treg cells

Shen

Jiang

Zhang

et al. 2021

Preprint

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Rheumatoid arthritis (RA) is a chronic and systemic autoimmune disease with the decreasing proportion of regulatory T (Treg) cells. Previous studies have shown that microRNAs (miRNAs, miR) act as key regulators of Treg cells. In this study, we assessed the involvement of miR-143-3p on Treg cells differentiation and function in the RA progress. We reported that the expression of miR-143-3p has been negatively associated with RA disease activity, and actively correlated with anti-inflammatory cytokine IL-10, which was secreted by Treg cells. In vitro, miR-143-3p expression in the CD4+T cells contributed to the upregulation of forkhead box protein 3 (Foxp3), which was the characteristic transcription factor of Treg cells. Notably, miR-143-3p mimics treatment markedly upregulated the frequency of Treg cells in vivo, effectively prevented CIA development and significantly inhibited inflammation in mice. Altogether, we proposed that MiR-143-3p can alleviate CIA by polarizing naive CD4+T cells into Treg cells, which warrants miR-143-3p as a target for the new therapeutic strategy of Treg-deficiency autoimmune diseases such as RA.

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Resistant starch intake alleviates collagen-induced arthritis in mice by modulating gut microbiota and promoting concomitant propionate production

Cited by 61 publications

References 57 publications

Dietary Derived Propionate Regulates Pathogenic Fibroblast Function and Ameliorates Experimental Arthritis and Inflammatory Tissue Priming

Dietary Derived Propionate Regulates Pathogenic Fibroblast Function and Ameliorates Experimental Arthritis and Inflammatory Tissue Priming

Bone Homeostasis and Gut Microbial-Dependent Signaling Pathways

MicroRNA-143-3p alleviates murine collagen-induced arthritis by polarizing naive CD4+T cells into Treg cells

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