2023
DOI: 10.1016/j.intimp.2023.110020
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Activated intestinal microbiome-associated tryptophan metabolism upregulates aryl hydrocarbon receptor to promote osteoarthritis in a rat model

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Cited by 6 publications
(12 citation statements)
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“…Of the 38 studies identified in this review, 24 were preclinical in vivo studies ( Table 2 ). Of these, 11 used an OA rat animal model (5 chemically induced OA [ 31 , 32 , 37 , 41 , 43 ], 1 surgically induced OA [ 36 ], 3 high fat diet-induced OA [ 34 , 42 , 44 ], 1 deoxycorticosterone acetate (DOCA) induced [ 46 ] and 1 antibiotic + tryptophan rich diet induced [ 40 ]), 11 used an OA mouse model (7 surgically induced OA [ 26 , 27 , 33 , 35 , 39 , 50 , 51 ], 2 high fat diet induced [ 44 , 45 ], 2 load induced [ 39 , 49 ], 1 used a spontaneous OA model in guinea pigs [ 52 ]) and 1 used a spontaneous OA model in rhesus macaques [ 47 ]. The number of animals used in these studies was variable (range: from 20 to 88) and not reported in a few articles ( n = 3) [ 26 , 31 , 38 ].…”
Section: Resultsmentioning
confidence: 99%
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“…Of the 38 studies identified in this review, 24 were preclinical in vivo studies ( Table 2 ). Of these, 11 used an OA rat animal model (5 chemically induced OA [ 31 , 32 , 37 , 41 , 43 ], 1 surgically induced OA [ 36 ], 3 high fat diet-induced OA [ 34 , 42 , 44 ], 1 deoxycorticosterone acetate (DOCA) induced [ 46 ] and 1 antibiotic + tryptophan rich diet induced [ 40 ]), 11 used an OA mouse model (7 surgically induced OA [ 26 , 27 , 33 , 35 , 39 , 50 , 51 ], 2 high fat diet induced [ 44 , 45 ], 2 load induced [ 39 , 49 ], 1 used a spontaneous OA model in guinea pigs [ 52 ]) and 1 used a spontaneous OA model in rhesus macaques [ 47 ]. The number of animals used in these studies was variable (range: from 20 to 88) and not reported in a few articles ( n = 3) [ 26 , 31 , 38 ].…”
Section: Resultsmentioning
confidence: 99%
“…The number of animals used in these studies was variable (range: from 20 to 88) and not reported in a few articles ( n = 3) [ 26 , 31 , 38 ]. The main technique used to assess OA was histology, which in some studies was also combined with specific semi-quantitative scores (Mankin’s and Osteoarthritis Research Society International (OARSI)) [ 26 , 33 , 37 , 39 , 40 , 50 ] and/or immunohistochemistry [ 33 , 46 ], ramp test [ 32 ], micro-computed tomography [ 27 , 32 , 46 , 49 , 51 ], anterior drawer test, Magnetic Resonance Imaging [ 47 ], and dual-energy X-ray absorptiometry [ 27 ]. Some articles ( n = 5) were designed to test the changes in the gut microbiota and metabolism during the administration of various supplements, such as quercetin, bioactive compounds from chicken cartilage, extracellular vesicles (EVs) from raw milk, oligofructose and prebiotic fiber, for OA [ 26 , 31 , 32 , 33 , 34 ].…”
Section: Resultsmentioning
confidence: 99%
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“…There is a relationship between their abnormal metabolism and the development and progression of OA [68,69]. First, abnormalities in the tryptophan metabolic pathway may lead to a shift of tryptophan to the synthetic pathway of inflammatory mediators, while reducing the utilization of tryptophan to the synthetic pathway in the growth and repair process, which may lead to damage of the osteoarticular cartilage [70,71]. In addition, tryptophan can be metabolized into serotonin, which has important effects on the growth and differentiation of articular cartilage cells [72], and a deficiency of serotonin may lead to articular cartilage damage [73,74].…”
Section: Discussionmentioning
confidence: 99%
“…Trp not only decreased the expression of pro-inflammatory factors Lj-TNF-α, Lj-IL-1β, and Lj-NF-κB, but also up-regulated the expression of anti-inflammatory factor Lj-TGF-β. A rat OA model was established using antibiotics models (without antibiotics as control) in combination with a high Trp diet to investigate the pathogenesis of OA by examining the aromatic receptor AhR family 1 cytochrome P450, polypeptide 1 (CyP1A1), bone and cartilage metabolic markers, inflammation, and gut microbial-associated Trp metabolites . The results showed that the severity of cartilaginous OA was positively correlated with the expression of AhR and CyP1A1 in chondrocytes, in which antibiotics reduced the relative abundance of cartilaginous lactic acid bacteria to alleviate synovial inflammation, and the high levels of Trp metabolism antagonized the effectiveness of antibiotics to exacerbate OA.…”
Section: Effects Of Trp Metabolites On Variety Of Diseasesmentioning
confidence: 99%