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Review
. 2022 Aug 10:12:935723.
doi: 10.3389/fcimb.2022.935723. eCollection 2022.

Gut microbiota remodeling: A promising therapeutic strategy to confront hyperuricemia and gout

Zhilei Wang  1   2 , Yuchen Li  3 , Wenhao Liao  1 , Ju Huang  2 , Yanping Liu  2 , Zhiyong Li  4 , Jianyuan Tang  1   2
Affiliations
Review

Gut microbiota remodeling: A promising therapeutic strategy to confront hyperuricemia and gout

Zhilei Wang et al. Front Cell Infect Microbiol. .

Abstract

The incidence of hyperuricemia (HUA) and gout continuously increases and has become a major public health problem. The gut microbiota, which colonizes the human intestine, has a mutually beneficial and symbiotic relationship with the host and plays a vital role in the host's metabolism and immune regulation. Structural changes or imbalance in the gut microbiota could cause metabolic disorders and participate in the synthesis of purine-metabolizing enzymes and the release of inflammatory cytokines, which is closely related to the occurrence and development of the metabolic immune disease HUA and gout. The gut microbiota as an entry point to explore the pathogenesis of HUA and gout has become a new research hotspot. This review summarizes the characteristics of the gut microbiota in patients with HUA and gout. Meanwhile, the influence of different dietary structures on the gut microbiota, the effect of the gut microbiota on purine and uric acid metabolism, and the internal relationship between the gut microbiota and metabolic endotoxemia/inflammatory factors are explored. Moreover, the intervention effects of probiotics, prebiotics, and fecal microbial transplantation on HUA and gout are also systematically reviewed to provide a gut flora solution for the prevention and treatment of related diseases.

Keywords: gout; gut microbiota; hyperuricemia; prebiotics; probiotics; uric acid.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Schematic diagram of the pathophysiological model of HUA and gout formation. HUA (serum UA levels >6.0 mg/dl) is caused by an imbalance of UA metabolism, including an increase in UA production through endogenous purine and exogenous purine metabolism and a decrease in UA excretion owing to the reduction of renal excretion and extrarenal excretion. The deposition of MSU crystals in or around the joints induces gout.
Figure 2
Figure 2
Diets affect the microbial composition of the gastrointestinal tract. High-fructose diet, high-fat diet, high-purine diet, etc. can lead to changes in the composition of intestinal flora in animal models of HUA and gout.
Figure 3
Figure 3
The mechanism of gut microbiota in UA and purine metabolism. The intestinal flora can affect purine metabolism, XOD, XDH, and urease activities, or the composition of SCFAs, and then alter the production and excretion of UA.
Figure 4
Figure 4
Intestinal flora affects the secretion of LPS and inflammatory response. Loss of gut barrier resulting from gut dysbiosis leads to gut-derived LPS translocation and chronic inflammation, resulting in the increase of SOD activity and serum UA. Moreover, gut microbiota can also modulate NLRP3 inflammasome activation, and the commensal microbiota shapes the ability of the host to respond to acute inflammatory stimuli that are dependent on the extra-intestinal inflammasome.
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