2024
DOI: 10.1016/j.bbi.2024.02.007
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A leaky gut dysregulates gene networks in the brain associated with immune activation, oxidative stress, and myelination in a mouse model of colitis

Jake Sondag Boles,
Maeve E. Krueger,
Janna E. Jernigan
et al.
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Cited by 4 publications
(3 citation statements)
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“…Mitochondrial dysfunction is also one of the contributing factors for increased oxidative stress, which can occur as a result of diminished mitophagy and an altered electron transport chain complex. , Environmental and occupational toxins that are known to induce PD, such as paraquat, rotenone, and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), predominantly act on the mitochondria and inhibit complex I of the electron transport chain and are frequently thought of as oxidative stressors. , Evidence gathered from animal and human post-mortem suggests that reactive oxygen and nitrogen species (ROS/RNS) are significant contributors in sporadic PD . Furthermore, coming to PNS, the gut epithelium itself induces the generation of ROS via formyl peptide receptors when it comes in contact with disturbed commensal microbiota or harmful bacteria finally causing the leaky gut state. , Additionally, Fasano reported that disrupted gut microbiota can disturb zonulin, which regulates antigen trafficking. As a result, luminal materials cross the epithelium and endothelium barrier, allowing a large inflow of food and microbial antigens that activate T cells.…”
Section: Pathophysiological Aspects: a Concise Overviewmentioning
confidence: 99%
See 1 more Smart Citation
“…Mitochondrial dysfunction is also one of the contributing factors for increased oxidative stress, which can occur as a result of diminished mitophagy and an altered electron transport chain complex. , Environmental and occupational toxins that are known to induce PD, such as paraquat, rotenone, and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), predominantly act on the mitochondria and inhibit complex I of the electron transport chain and are frequently thought of as oxidative stressors. , Evidence gathered from animal and human post-mortem suggests that reactive oxygen and nitrogen species (ROS/RNS) are significant contributors in sporadic PD . Furthermore, coming to PNS, the gut epithelium itself induces the generation of ROS via formyl peptide receptors when it comes in contact with disturbed commensal microbiota or harmful bacteria finally causing the leaky gut state. , Additionally, Fasano reported that disrupted gut microbiota can disturb zonulin, which regulates antigen trafficking. As a result, luminal materials cross the epithelium and endothelium barrier, allowing a large inflow of food and microbial antigens that activate T cells.…”
Section: Pathophysiological Aspects: a Concise Overviewmentioning
confidence: 99%
“…36 Furthermore, coming to PNS, the gut epithelium itself induces the generation of ROS via formyl peptide receptors when it comes in contact with disturbed commensal microbiota or harmful bacteria finally causing the leaky gut state. 37,38 Additionally, Fasano reported that disrupted gut microbiota can disturb zonulin, which regulates antigen trafficking. As a result, luminal materials cross the epithelium and endothelium barrier, allowing a large inflow of food and microbial antigens that activate T cells.…”
Section: Pathophysiological Aspects: a Concise Overviewmentioning
confidence: 99%
“…This complex network involves the neural, endocrine, and immune systems [13][14][15][16][17]. The intricate information exchanged between the CNS and the gut microbiome is mediated by microbiome-derived products, including serotonin, dopamine, norepinephrine, shortchain fatty acids (SCFAs), glutamate, γ-aminobutyric acid (GABA), secondary bile acids, tryptophan metabolites, and histamine.…”
Section: Introductionmentioning
confidence: 99%