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高尿酸血症中的肠道微生物失调通过激活 NLRP3 炎性体促进肾损伤。

Gut microbiota dysbiosis in hyperuricaemia promotes renal injury through the activation of NLRP3 inflammasome.

机构信息

Zhujiang Hospital of Southern Medical University, Guangzhou, 510280, China.

School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.

出版信息

Microbiome. 2024 Jun 21;12(1):109. doi: 10.1186/s40168-024-01826-9.

DOI:10.1186/s40168-024-01826-9
PMID:38907332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11191305/
Abstract

BACKGROUND: The prevalence of hyperuricaemia (HUA), a metabolic disorder characterized by elevated levels of uric acid, is on the rise and is frequently associated with renal injury. Gut microbiota and gut-derived uremic toxins are critical mediators in the gut-kidney axis that can cause damage to kidney function. Gut dysbiosis has been implicated in various kidney diseases. However, the role and underlying mechanism of the gut microbiota in HUA-induced renal injury remain unknown. RESULTS: A HUA rat model was first established by knocking out the uricase (UOX). HUA rats exhibited apparent renal dysfunction, renal tubular injury, fibrosis, NLRP3 inflammasome activation, and impaired intestinal barrier functions. Analysis of 16S rRNA sequencing and functional prediction data revealed an abnormal gut microbiota profile and activation of pathways associated with uremic toxin production. A metabolomic analysis showed evident accumulation of gut-derived uremic toxins in the kidneys of HUA rats. Furthermore, faecal microbiota transplantation (FMT) was performed to confirm the effects of HUA-induced gut dysbiosis on renal injury. Mice recolonized with HUA microbiota exhibited severe renal injury and impaired intestinal barrier functions following renal ischemia/reperfusion (I/R) surgery. Notably, in NLRP3-knockout (NLRP3) I/R mice, the deleterious effects of the HUA microbiota on renal injury and the intestinal barrier were eliminated. CONCLUSION: Our results demonstrate that HUA-induced gut dysbiosis contributes to the development of renal injury, possibly by promoting the production of gut-derived uremic toxins and subsequently activating the NLRP3 inflammasome. Our data suggest a potential therapeutic strategy for the treatment of renal diseases by targeting the gut microbiota and the NLRP3 inflammasome. Video Abstract.

摘要

背景：高尿酸血症（HUA）是一种代谢紊乱，其特征是尿酸水平升高，并且经常与肾损伤有关。肠道微生物群和肠道来源的尿毒症毒素是肠道-肾脏轴的关键介质，可导致肾功能损害。肠道菌群失调与各种肾脏疾病有关。然而，肠道微生物群在 HUA 诱导的肾损伤中的作用和潜在机制尚不清楚。

结果：首先通过敲除尿酸酶（UOX）建立 HUA 大鼠模型。HUA 大鼠表现出明显的肾功能障碍、肾小管损伤、纤维化、NLRP3 炎性体激活和肠道屏障功能受损。16S rRNA 测序和功能预测数据分析显示，肠道微生物群谱异常，与尿毒症毒素产生相关的途径被激活。代谢组学分析显示 HUA 大鼠肾脏中明显积累了肠道来源的尿毒症毒素。此外，进行粪便微生物群移植（FMT）以确认 HUA 诱导的肠道菌群失调对肾损伤的影响。用 HUA 微生物群重新定植的小鼠在肾缺血/再灌注（I/R）手术后表现出严重的肾损伤和肠道屏障功能受损。值得注意的是，在 NLRP3 敲除（NLRP3）I/R 小鼠中，HUA 微生物群对肾损伤和肠道屏障的有害影响被消除。

结论：我们的结果表明，HUA 诱导的肠道菌群失调导致肾损伤的发展，可能通过促进肠道来源的尿毒症毒素的产生，随后激活 NLRP3 炎性体。我们的数据表明，通过靶向肠道微生物群和 NLRP3 炎性体，为治疗肾脏疾病提供了一种潜在的治疗策略。视频摘要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/61d8c913a696/40168_2024_1826_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/d52904de30a7/40168_2024_1826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/be6de7e5ffa3/40168_2024_1826_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/8ba16e8f7617/40168_2024_1826_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/b0cc21c526d3/40168_2024_1826_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/aa1b165c9f81/40168_2024_1826_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/6a976adc6e5f/40168_2024_1826_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/61d8c913a696/40168_2024_1826_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/d52904de30a7/40168_2024_1826_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/be6de7e5ffa3/40168_2024_1826_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/8ba16e8f7617/40168_2024_1826_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/b0cc21c526d3/40168_2024_1826_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/aa1b165c9f81/40168_2024_1826_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/6a976adc6e5f/40168_2024_1826_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4529/11191305/61d8c913a696/40168_2024_1826_Fig7_HTML.jpg

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[3]
Mechanisms of NLRP3 inflammasome in chronic kidney disease and the effects of traditional Chinese medicines.

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[4]
The influence of gut microbiota on the gut-brain-kidney axis and its implications for chronic kidney disease.

Front Microbiol. 2025-7-9

[5]
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BMC Microbiol. 2025-7-10

[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Perturbed gut microbiome and fecal and serum metabolomes are associated with chronic kidney disease severity.

Microbiome. 2023-1-9

[2]
Intestinal dysbiosis mediates cognitive impairment via the intestine and brain NLRP3 inflammasome activation in chronic sleep deprivation.

Brain Behav Immun. 2023-2

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Alteration of Gut Microbiome and Correlated Amino Acid Metabolism Contribute to Hyperuricemia and Th17-Driven Inflammation in -KO Mice.

Front Immunol. 2022

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Adv Nutr. 2021-7-30

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