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240114s2024 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2024.109903
|2 doi
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|a pubmed25n1223.xml
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|a (DE-627)NLM36708760X
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|a (NLM)38218211
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|a (PII)S1521-6616(24)00014-7
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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|a Liu, Jing
|e verfasserin
|4 aut
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|a Short-chain fatty acids ameliorate experimental anti-glomerular basement membrane disease
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
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|a Date Completed 29.01.2024
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|a Date Revised 10.04.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2024 Elsevier Inc. All rights reserved.
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|a BACKGROUND: Short-chain fatty acids (SCFAs), as the link between gut microbiota and the immune system, had been reported to be protective in many autoimmune diseases by the modulation of T cell differentiation. The pathogenic role of autoreactive Th1 and Th17 cells and the protective role of Treg cells in the pathogenesis of anti-GBM disease have been fully demonstrated. Thus, the present study aimed to investigate the therapeutic effects of SCFAs in a rat model of anti-GBM disease
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|a MATERIALS AND METHODS: Experimental anti-GBM disease was constructed by immunizing Wistar Kyoto rats with a nephrogenic T cell epitope α3127-148, and intervened by sodium acetate, sodium propionate, or sodium butyrate, 150 mM in the drinking water from day 0 to 42. Kidney injury was accessed by the biochemical analyzer, immunofluorescence, and immunohistochemistry. Antibody response was detected by ELISA. T cell clustering and proliferation were detected by flow cytometry. Human kidney 2 (HK2) cells were stimulated in vitro and cytokines were assessed by quantitative real-time PCR
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|a RESULTS: Treatment with sodium acetate, sodium propionate, or sodium butyrate ameliorated the severity of kidney impairment in rats with anti-GBM glomerulonephritis. In the sodium butyrate-treated rats, the urinary protein, serum creatinine, and blood urea nitrogen levels were significantly lower; the percentage of crescent formation in glomeruli was significantly reduced; and the kidneys showed reduced IgG deposition, complement activation, T cell, and macrophage infiltration as well as the level of circulating antibodies against anti-α3(IV)NC1. The treatment of sodium butyrate reduced the α3127-148-specific T cell activation and increased the Treg cells differentiation and the intestinal beneficial bacteria flora. It also alleviated the damage of HK2 cells treated with inflammatory factors and complement
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|a CONCLUSION: Treatment with SCFAs, especially butyrate, alleviated anti-GBM nephritis in rat model, indicating its potential therapeutic effects in clinical usage
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Anti-GBM disease
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|a Immunity
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|a Inflammation
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|a Short-chain fatty acids
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|a sodium propionate
|2 NLM
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|a DK6Y9P42IN
|2 NLM
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|a Butyric Acid
|2 NLM
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|a 107-92-6
|2 NLM
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|a Sodium Acetate
|2 NLM
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|a 4550K0SC9B
|2 NLM
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|a Propionates
|2 NLM
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1 |
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|a Gu, Qiu-Hua
|e verfasserin
|4 aut
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1 |
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|a Cui, Zhao
|e verfasserin
|4 aut
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1 |
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|a Zhao, Ming-Hui
|e verfasserin
|4 aut
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|a Jia, Xiao-Yu
|e verfasserin
|4 aut
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 259(2024) vom: 01. Feb., Seite 109903
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnas
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|g volume:259
|g year:2024
|g day:01
|g month:02
|g pages:109903
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|u http://dx.doi.org/10.1016/j.clim.2024.109903
|3 Volltext
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