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. 2022 Dec 8;9:1060581. doi: 10.3389/fmed.2022.1060581

FIGURE 1.

FIGURE 1

Mechanisms by which FMT restores negative changes in metabolic disease, neuropsychiatric conditions and inflammatory bowel disease. (A) LPS-mediated increases in IL-1, TNF-α, and IL-6 leads to metabolic endotoxemia decreasing insulin sensitivity in liver, adipose, and muscle tissue. FMT reduces LPS, IL-1 and TNF-α, lowers serum glucose, HgbA1c and cholesterol levels and preserves beta-cells in T1DM patients. FMT increases Eubacterium, Lactobacillus, and Bifidobacterium spp., while reducing Desulfovibrio and Bilophila spp. (B) FMT increases dopamine transporter and serotonin transporter expression, while also increasing Bacteroides and Alistipes in patients in depression. FMT increase Lactobacillus, Bifidobacterium and Treg activity in multiple sclerosis patients, while reducing relapses/flares. FMT increases synapsin, amyloid plaques and Tau-protein phosphorylation in Alzheimer’s disease while reducing Desulfovibrio spp. FMT increases dopamine while decreasing neuroinflammation, motor and non-motor symptoms in Parkinson’s disease. FMT increases Bifidobacterium spp. and reduces p-cresol and Desulfovibrio spp. in autism spectrum disorder. (C) Inflammatory bowel disease is characterized by increased gut inflammation, intestinal permeability and Ruminococcus spp. with decreased Eubacterium, Lactobacillus, Bifidobacterium, Faecalibacterium, Treg activity and SCFA. FMT restores Eubacterium and Faecalibacterium, increases Treg activity, while decreasing Escherichia spp., Fusobacterium, Streptococcus, intestinal permeability, and pro-inflammatory cytokines. IL-1, interleukin-1; TNF-α, tumor necrosis factor α; IL-6, interleukin-6; LPS, lipopolysaccharides; FMT, fecal microbiota transplant; HgbA1c, hemoglobin A1c; MS, multiple sclerosis; DAT, dopamine transporter; SERT, serotonin transporter; Treg, T-regulatory; SCFA, short-chain fatty acids.