Shirvani-Rad Salman, Khatibzade-Nasari Niloufar, Ejtahed Hanieh-Sadat, Larijani Bagher
Microbiota Research Group, Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Faculty of Medicine, Qeshm International Medical Sciences Branch, Islamic Azad University, Qeshm, Iran.
Front Med (Lausanne). 2023 May 17;10:1163778. doi: 10.3389/fmed.2023.1163778. eCollection 2023.
Gut dysbiosis is believed to be one of the several mechanisms that are involved in the pathogenesis of gout. This systematic review aimed to summarize the role of gut dysbiosis in gout disease and uncover the underlying mechanisms.
A comprehensive search was conducted on PubMed, Web of Science, and Scopus databases up to October 2021. Animal studies and human observational studies, including case-control, cross-sectional, and cohort studies assessing the association between gut microbiota composition and gout were included. The quality of included studies has been evaluated using the Newcastle-Ottawa Quality Assessment scale (NOS) and the SYRCLE's risk of bias tool.
Initially, we found 274 studies among which 15 studies were included in this systematic review. Of them, 10 studies were conducted on humans and 5 studies were conducted on animals. Increased abundance of and decreased abundance of alters purine metabolism, thereby aggravating gout condition. Moreover, a higher abundance of and in gout modulates enzymatic activity in purine metabolism. Butyrate-producing bacteria such as , and have higher abundance in healthy controls compared to gout patients, suggesting the anti-inflammatory and anti-microbial role of short-chain fatty acids (SCFAs). Lipopolysaccharides (LPS)-releasing bacteria, such as e, , and , are also involved in the pathogenesis of gout disease by stimulating the innate immune system.
Exploring the role of gut dysbiosis in gout and the underlying mechanisms can help develop microbiota-modulating therapies for gout.
肠道菌群失调被认为是痛风发病机制中涉及的多种机制之一。本系统评价旨在总结肠道菌群失调在痛风疾病中的作用,并揭示其潜在机制。
截至2021年10月,对PubMed、Web of Science和Scopus数据库进行了全面检索。纳入动物研究和人类观察性研究,包括病例对照研究、横断面研究和队列研究,以评估肠道微生物群组成与痛风之间的关联。使用纽卡斯尔-渥太华质量评估量表(NOS)和SYRCLE偏倚风险工具对纳入研究的质量进行了评估。
最初,我们发现了274项研究,其中15项研究被纳入本系统评价。其中,10项研究是针对人类进行的,5项研究是针对动物进行的。[具体细菌名称1]丰度增加和[具体细菌名称2]丰度降低会改变嘌呤代谢,从而加重痛风病情。此外,痛风患者中[具体细菌名称3]和[具体细菌名称4]丰度较高会调节嘌呤代谢中的酶活性。与痛风患者相比,健康对照中产生丁酸盐的细菌,如[具体细菌名称5]、[具体细菌名称6]和[具体细菌名称7]丰度更高,这表明短链脂肪酸(SCFAs)具有抗炎和抗菌作用。释放脂多糖(LPS)的细菌,如[具体细菌名称8]、[具体细菌名称9]和[具体细菌名称10],也通过刺激先天免疫系统参与痛风疾病的发病机制。
探索肠道菌群失调在痛风中的作用及其潜在机制有助于开发针对痛风的微生物群调节疗法。