Gut microbiota and obesity-associated osteoarthritis

Liu, Y.; Ding, Wei; Wang, H.L.; Dai, Lulu; Zong, Wenhao; Wang, Y.Z.; Bi, Joffe; Han, Weiyu; Dong, Guijun

doi:10.1016/j.joca.2019.05.009

Cited by 65 publications

(45 citation statements)

References 103 publications

(127 reference statements)

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“…Finally, the butyrate-acetoacetate CoA-transferase was enriched in obese subjects, resulting in an excess of energy accumulation. These findings are in line with previous data in the literature showing a correlation between the development of obesity-associated OA and gut dysbiosis [58,59] in animal models, acting through an interaction with the innate immune system at both systemic and local levels [59]. Lipotoxicity is a typical feature of the metabolic syndrome that might promote the production of proinflammatory cytokines with the consequent recruitment of mast cells, macrophages, and dendritic cells in the adipose tissue, inducing a chronic low-grade inflammatory status [60].…”

Section: Obesity and Metabolic Syndromesupporting

confidence: 93%

Gut–Joint Axis: The Role of Physical Exercise on Gut Microbiota Modulation in Older People with Osteoarthritis

Sire

Petito

et al. 2020

Nutrients

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Osteoarthritis (OA) is considered one of the most common joint disorders worldwide and its prevalence is constantly increasing due to the global longevity and changes in eating habits and lifestyle. In this context, the role of gut microbiota (GM) in the pathogenesis of OA is still unclear. Perturbation of GM biodiversity and function, defined as ‘gut dysbiosis’, might be involved in the development of inflammaging, one of the main risk factors of OA development. It is well known that physical exercise could play a key role in the prevention and treatment of several chronic diseases including OA, and it is recommended by several guidelines as a first line intervention. Several studies have shown that physical exercise could modulate GM composition, boosting intestinal mucosal immunity, increasing the Bacteroidetes–Firmicutes ratio, modifying the bile acid profile, and improving the production of short chain fatty acids. Moreover, it has been shown that low intensity exercise might reduce the risk of gastrointestinal diseases, confirming the hypothesis of a strict correlation between skeletal muscle and GM. However, up to date, there is still a lack of clinical trials focusing on this research field. Therefore, in this narrative, we aimed to summarize the state-of-the-art of the literature regarding the correlation between these conditions, supporting the hypothesis of a ‘gut–joint axis’ and highlighting the role of physical exercise combined with adequate diet and probiotic supplements in rebalancing microbial dysbiosis.

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Section: Obesity and Metabolic Syndromesupporting

confidence: 93%

Gut–Joint Axis: The Role of Physical Exercise on Gut Microbiota Modulation in Older People with Osteoarthritis

Sire

Petito

et al. 2020

Nutrients

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“…For knee OA, enough evidence indicates that there are a number of moderate to strong risk factors, including menopause and previous knee injury [3,4], and it is associated with metabolic diseases, such as severe obesity [5]. Imbalances in the gut microbiota, which are the bacteria that inhabit the intestines, are also major pathogenic mechanisms of obesity [6].…”

Section: Introductionmentioning

confidence: 99%

Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

et al. 2020

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Gut microbiota dysbiosis has been studied under the pathological conditions of osteoarthritis (OA). However, the effect of antibiotic-induced gut flora dysbiosis on OA remains incompletely understood at present. Herein, we used a mouse (8 weeks) OA model of destabilization of the medial meniscus (DMM) and gut microbiome dysbiosis induced by antibiotic treatment with ampicillin and neomycin for 8 weeks. The results show that antibiotic-induced intestinal microbiota dysbiosis reduced the serum level of lipopolysaccharide (LPS) and the inflammatory response, such as suppression of the levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which can lead to decreased matrix metalloprotease-13 (MMP-13) expression and improvement of OA after joint injury. In addition, trabecular thickness (Tb.Th) and osteophyte scores were increased significantly in antibiotic-induced male mice compared with female mice. We further used network correlation analysis to verify the effect of gut microbiota dysbiosis on OA. Therefore, this study contributes to our understanding of the gut-joint axis in OA and reveals the relationship between the inflammatory response, sex and gut microbiota, which may provide new strategies to prevent the symptoms and long-term sequelae of OA.

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“…There is growing evidence that perturbation of commensal intestinal microbiota is involved in the pathogenesis of various diseases including rheumatoid arthritis, obesity, and osteoporosis (44)(45)(46). Furthermore, changes in the gut microbiome and chronic systemic inflammation due to obesity can accelerate OA development (47,48). Obesity-induced synovial inflammation, chondrocyte hypertrophy, and meniscal mineralization are mitigated through oligofructose, a non-digestible prebiotic fiber that facilitates the expansion of beneficial Bifidobacteria and improves insulin resistance (49).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1-Interleukin-17 Signaling Axis Induces Cartilage Destruction and Promotes Experimental Osteoarthritis

Na¹,

Park²,

Cho³

et al. 2020

Front. Immunol.

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Osteoarthritis (OA), which is the most common degenerative joint disorder, has been considered a non-inflammatory disease with abnormal mechanics. Interleukin (IL)-17 is a pleiotropic cytokine involved in inflammatory diseases and their production is driven by the cytokine including IL-1 and IL-23. However, little is known about the mechanism of IL-17 in the development of OA. Here, we investigated the role of IL-17 in the pathogenesis of OA using monosodium iodoacetate (MIA)-injected IL-17 and IL-1 receptor antagonist (IL-1Ra) double-deficient mice. In MIA-injected IL-1Ra KO mice, nociceptive properties, degree of cartilage damage, and the level of inflammatory factors in articular cartilage were increased compared to MIA-injected wild-type mice. Interestingly, the intestinal architecture was impaired in IL-1Ra KO mice compared to wild-type mice and the damage was further exacerbated by MIA injection. Deficiency of IL-17 reduced nociceptive properties and cartilage destruction, as well as inflammationrelated factors in MIA-injected IL-1Ra KO mice compared to MIA-injected wild-type mice. Furthermore, IL-17-treated chondrocytes from OA patients showed enhanced expression of catabolic factors that are involved in the destruction of cartilage in OA. IL-17 accelerates the destruction of cartilage and small intestine via regulation of several inflammatory mediators in an OA murine model. These results suggest that IL-17 plays a critical role in the development of OA.

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Gut microbiota and obesity-associated osteoarthritis

Cited by 65 publications

References 103 publications

Gut–Joint Axis: The Role of Physical Exercise on Gut Microbiota Modulation in Older People with Osteoarthritis

Gut–Joint Axis: The Role of Physical Exercise on Gut Microbiota Modulation in Older People with Osteoarthritis

Gut microbiome dysbiosis alleviates the progression of osteoarthritis in mice

Interleukin-1-Interleukin-17 Signaling Axis Induces Cartilage Destruction and Promotes Experimental Osteoarthritis

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