Figure 1.

Interactions between gut microbiota and gout. The diversity and abundance of gut microbiota change include the increase of Prevotella and Bacteroides and the decrease of Enterobacteriaceae, Faecalibacterium, the microbiota with the allantoinase gene, Clostridium, and Ruminococcus. These changes result in excessive uric acid production in the liver and insufficient uric acid excretion in the kidney and intestine, raising serum uric acid levels above normal. In addition, some microbiota with the allantoinase and the xanthine dehydrogenase gene changed in gout can directly regulate the intestinal uric acid levels. However, the contribution of elevated intestinal uric acid levels to elevated serum uric acid levels remains unknown. Consequently, occludin and claudin-1 levels at tight epithelial junctions can drop when serum uric acid levels rise. Gout is caused by inflammation-related bacteria that upregulate TLR2/4/5 and encourage the release of IL-1 β and TNF- α. However, some SCFAs may have a protective role in inflammation. SCFAs, especially butyrate, are associated with the increased expression of Inhibitory-κκBα (I-κBα), which inhibits the phosphorylation and nuclear translocation of NF-κB p65, and the downstream inflammatory cytokine, MCP-1, and IL-1β expression.