Figure 1.
The proposed effects of the bioactive compounds found in medicinal mushrooms on the composition of the gut microbiota, the production of microbial metabolites, the integrity of the intestinal barrier, immune regulation, and gut-brain axis signalling. [1]
Table 1.
Summary of studies investigating the effects of medicinal mushrooms on gut microbiota composition, intestinal barrier integrity, inflammation, and gut–brain axis-related outcomes.
| Mushroom / Reference | Study Model | Intervention / Dosage | Key Gut Microbiota Changes | Key Metabolic & Inflammatory Outcomes |
|---|---|---|---|---|
| Hericium erinaceus | ||||
| Xie et al. (2021) [15] | Human pilot study; healthy adults (n=13) | H. erinaceus powder, 3 g/day, 7 days | ↑ alpha diversity; ↑ Faecalibacterium prausnitzii, Eubacterium rectale, Fusicatenibacter saccharivorans, Gemmiger formicilis, Kineothrix alysoides; ↓ Streptococcus thermophilus, Bacteroides caccae, Romboutsia timonensis | No adverse effects; correlations with LDL, uric acid, creatinine, and ALP |
| Yang et al. (2021) [16] | Mice; young and middle-aged Kunming mice (n=42) | Polysaccharides, 500 or 1000 mg/kg, 28 days | ↑ Lachnospiraceae, Akkermansiaceae; ↓ Rikenellaceae, Bacteroidaceae | ↓ body weight gain; ↑ NO, IL-6, IL-10, TNF-α, IFN-γ; activation of NF-κB, MAPK, and PI3K/Akt pathways |
| Ren et al. (2023) [12] | Cynomolgus macaques with ulcerative colitis (n=15) | Mycelial polysaccharide, ∼500 mg/kg/day, 4 weeks | ↑ richness and diversity; ↑ Methanobrevibacter smithii, Lactobacillus reuteri; ↓ Streptococcus lutetiensis | ↓ diarrhea; improved histopathology and nutritional status |
| Bei et al. (2026) [9] | Rats; ethanol-induced gastric injury (n=42) | Aqueous or ethanolic extract, 150–250 mg/kg | ↑ SCFA-producing bacteria (Blautia, Fusicatenibacter, Acetitomaculum) | ↑ propionate; ↓ 12(S)-HETE; protection against gastric mucosal injury |
| Priori et al. (2024) [8] | Aged mice | Extract 1 mg/mouse/day, 2 months | Beneficial microbiota modulation | ↓ neuroinflammation; improved cognitive performance |
| Ganoderma lucidum (Reishi) | ||||
| Chang et al. (2015) [4] | HFD-induced obese mice | Water extract of mycelium (WEGL), 2–8%, 8 weeks | ↓ Firmicutes/Bacteroidetes ratio; ↓ Mucispirillum schaedleri, Escherichia fergusonii, Enterococcus faecalis; ↑ Parabacteroides goldsteinii, Roseburia hominis, Bacteroides spp. | ↓ adiposity, hepatic steatosis, endotoxemia; ↓ TLR4/JNK/NF-κB signaling; FMT reproduced metabolic benefits |
| Guo et al. (2021) [5] | AOM/DSS-induced colorectal cancer in mice | Polysaccharide (GLP), 200–300 mg/kg | ↑ diversity; ↑ SCFA producing taxa | ↓ tumour burden; ↑ propionate and butyrate; ↑ ZO-1, occludin, GPR43; ↓ LPS and TLR4/MyD88/NF-κB signaling |
| Li et al. (2022) [17] | DSS-induced colitis in mice | Ethanolic extract (GLE), 50–100 mg/kg | ↑ Bifidobacterium, Turicibacter; ↓ Staphylococcus, Romboutsia | ↓ TNF-α, IL-1β, IL-6, IL-17, iNOS, COX-2; ↑ IL-10, PPAR-γ; ↑ MUC2, ZO-1, occludin |
| Cordyceps militaris | ||||
| Lee et al. (2021) [10] | HFSD-induced metabolic dysfunction in mice | Fruiting body, polysaccharides, cordycepin-rich fraction, 8 weeks | ↑ Akkermansia; ↓ HFSD-associated dysbiosis | ↓ glucose; ↓ triglycerides; ↑ intestinal mucus production |
| Wu et al. (2023) [14] | DSS-induced colitis in mice (n=32) | Powder, 100 or 300 mg/kg/day, 14 days | ↑ Lactobacillus, Limosilactobacillus, Ligilactobacillus, Odoribacter | ↓ DAI, TNF-α, IL-1β; ↑ MUC2, ZO-1, claudin-1, occludin; improved histology |
| Jing et al. (2023) [6] | Chronic stress model in mice | Cordycepin, 12.5–25 mg/kg, 4 weeks | Reversal of stress-induced dysbiosis; modulation of NK4A214 group, Prevotellaceae_UCG-001, Desulfovibrio | ↓ corticosterone, IFN-γ, IL-1β; improved anxiety and depression-like behaviors |
| Phellinus linteus | ||||
| Liu et al. (2020) [18] | Type 2 diabetic rats | PLPE, 600 mg/kg/day, 8 weeks | ↑ Roseburia, Prevotella_9, Blautia, Oscillibacter; ↓ Escherichia-Shigella, Clostridium sensu stricto 1 | ↓ glucose, HOMA IR, LPS, TNF-α, IL-6, CRP; ↑ propionate, butyrate; ↑ ZO-1, occludin, claudin-1 |
| Liu et al. (2023) [11] | In vitro fecal fermentation model | PLP, 50 mg/mL, 48 h fermentation | ↑ richness; ↑ Bacteroides, Parabacteroides, Prevotella, Butyricimonas; ↓ Escherichia-Shigella, Morganella | ↑ acetate, propionate, butyrate; modulation of bile acid, amino acid, and purine metabolism |
[i] Abbreviations: ↑ increase; ↓ decrease; AOM, azoxymethane; ALP, alkaline phosphatase; CRP, C-reactive protein; DSS, dextran sulfate sodium; FMT, fecal microbiota transplantation; GLE, Ganoderma lucidum ethanolic extract; GLP, Ganoderma lucidum polysaccharide; HFD, high-fat diet; HFSD, high-fat/high-sucrose diet; HOMA-IR, homeostatic model assessment of insulin resistance; IL, interleukin; LDL, low-density lipoprotein; LPS, lipopolysaccharide; PLP, Phellinus linteus polysaccharide; PLPE, Phellinus linteus polysaccharide extract; SCFA, short-chain fatty acid; TNF-α, tumour necrosis factor-α; WEGL, water extract of Ganoderma lucidum mycelium; In Yang et al. (2021), the increase in IL-6, TNF-α, IFN-γ, and NO reflects physiological immunostimulation in healthy animals rather than a pro-inflammatory state.
Figure 2.
Proposed mechanisms of action of medicinal mushrooms on the gut microbiota–gut–brain axis. (SCFA – short-chain fatty acids; LPS – lipopolysaccharide; ZO-1 – zonula occludens-1; TNF-α – tumour necrosis factor-α; IL – interleukin; MUC2 – mucin 2)