β-Glucan-rich Hericium erinaceus hot-water extract ameliorates acute colitis by suppressing inflammation, preserving the epithelial barrier, and modulating gut microbiota ecosystem.

HE-HW was found to be rich in 1,3:1,6-β-glucan at a concentration of 286.4 mg/g.

• The extract was characterized as a β-glucan-rich hot-water extract of Hericium erinaceus (HE-HW).
• The specific glucan type identified was 1,3:1,6-β-glucan at 286.4 mg/g.
• This commercially relevant extract was studied to address a translational gap compared to isolated polysaccharides.

HE-HW suppressed lipopolysaccharide-induced nitric oxide and pro-inflammatory cytokines in RAW 264.7 macrophages without cytotoxicity.

• HE-HW was tested at concentrations of 1–10 μg/mL in RAW 264.7 macrophages.
• The extract suppressed LPS-induced nitric oxide production.
• Pro-inflammatory cytokines suppressed included IL-6 and MCP-1.
• No cytotoxicity was observed at the tested concentrations.

HE-HW downregulated inflammatory mediators and restored tight junction gene expression in DSS-stimulated Caco-2 cells.

• Caco-2 intestinal epithelial cells were stimulated with DSS to model epithelial barrier disruption.
• HE-HW treatment downregulated inflammatory mediators in the DSS-stimulated cells.
• Tight junction genes restored included occludin, ZO-1, and MUC2.
• These findings suggest HE-HW can reinforce epithelial barrier integrity at the gene expression level.

Oral administration of HE-HW improved disease activity and colon length in DSS-induced colitis mice.

• HE-HW was administered orally at doses of 1 or 5 mg/kg/day in the mouse colitis model.
• Treatment improved disease activity index scores in DSS-induced colitis mice.
• Colon length, which is reduced in colitis, was improved with HE-HW treatment.
• Both serum and tissue cytokines and immunoglobulins were normalized with treatment.

Histological analysis confirmed that HE-HW reduced mucosal damage, muscle thickening, and collagen accumulation in DSS-induced colitis mice.

• Histology was performed on colon tissue from DSS-induced colitis mice treated with HE-HW.
• Reduced mucosal damage was observed in HE-HW-treated mice compared to DSS controls.
• Muscle thickening and collagen accumulation, indicators of fibrotic remodeling, were also reduced.
• These histological findings were observed at oral doses of 1 or 5 mg/kg/day.

HE-HW attenuated DSS-associated enrichment of specific inflammation-related gut microbial taxa, including Erysipelatoclostridium, Faecalibaculum, and Olsenella.

• Gut microbiome profiling was conducted in DSS-induced colitis mice treated with HE-HW.
• DSS treatment was associated with enrichment of Erysipelatoclostridium, Faecalibaculum, and Olsenella.
• HE-HW treatment attenuated the enrichment of these inflammation-related microbial populations.
• The authors described this effect as 'selective remodeling of inflammation-related microbial populations.'
• Microbiota modulation was identified as one of three primary mechanisms by which HE-HW confers protection against colitis.