Alginate alleviates hyperuricemia by modulating the Pediococcus acidilactici LW1-1-butyrate-NLRP3 inflammasome axis.

2026-04
International journal of biological macromolecules 354

PubMed: 41819315
DOI: 10.1016/j.ijbiomac.2026.151318

Study Design

Population: HUA mice
Methods: Alg administration; from alginate-treated HUA mice, Pediococcus acidilactici LW1-1 was isolated using a high-UA selective medium; in vivo, P. acidilactici LW1-1 and butyrate were tested for effects on intestinal inflammation, barrier dysfunction, and urate excretion

Animal Study

Hyperuricemia (HUA) is a prevalent metabolic disorder and a growing global health concern, in which the gut microbiota plays a critical role in uric acid (UA) metabolism. In this study, alginate (Alg; Mw: 60 kDa, G/M = 1.80), a marine-derived polysaccharide composed of α-L-guluronic acid and β-D-mannuronic acid, was investigated for its protective effects against HUA. Alg administration significantly reduced serum UA levels and alleviated HUA-associated body weight loss. Mechanistically, Alg reshaped gut microbial dysbiosis, particularly by selectively enriching lactic acid bacteria. From alginate-treated HUA mice, Pediococcus acidilactici LW1-1 was isolated using a high-UA selective medium. In vivo, P. acidilactici LW1-1 enriched butyrate-producing bacteria and increased butyrate levels, thereby protecting against intestinal inflammation and barrier dysfunction. Both P. acidilactici LW1-1 and butyrate suppressed intestinal inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation and enhancing tight junction integrity. Concurrently, these interventions upregulated expression of the urate efflux transporter ATP-binding cassette subfamily G member 2 (ABCG2) in the intestine and kidney, thereby promoting UA excretion via dual pathways. Collectively, our findings highlight the therapeutic potential and safety of the polysaccharide-microbiota-metabolite axis in HUA and propose a novel microbiota-targeted strategy for managing HUA through probiotic and prebiotic interventions.

Research Insights

Supplement	Dose	Health Outcome	Effect Type	Effect Size	Source
Pediococcus acidilactici	—	Improved Intestinal Barrier Function	Beneficial	Moderate	View source P. acidilactici LW1-1 enriched butyrate-producing bacteria and increased butyrate levels, thereby protecting against intestinal inflammation and barrier dysfunction... Both P. acidilactici LW1-1 and butyrate suppressed intestinal inflammation by inhibiting NLRP3 inflammasome activation and enhancing tight junction integrity.
Pediococcus acidilactici	—	Increased Uric Acid Excretion	Beneficial	Moderate	View source Concurrently, these interventions upregulated expression of the urate efflux transporter ATP-binding cassette subfamily G member 2 (ABCG2) in the intestine and kidney, thereby promoting UA excretion via dual pathways.
Pediococcus acidilactici	—	Reduced Intestinal Inflammation	Beneficial	Moderate	View source Both P. acidilactici LW1-1 and butyrate suppressed intestinal inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation and enhancing tight junction integrity.
Pediococcus acidilactici	—	Reduced Uric Acid Levels	Beneficial	Large	View source P. acidilactici LW1-1 enriched butyrate-producing bacteria and increased butyrate levels, thereby protecting against intestinal inflammation and barrier dysfunction... Concurrently, these interventions upregulated expression of the urate efflux transporter ABCG2 in the intestine and kidney, thereby promoting UA excretion via dual pathways.