Our work suggests that protein misfolding and immune activation in neurodegenerative disorders are triggered through cross-seeding by exposure to exogenous microbial amyloids in the nose, mouth and gut.
Streptococcus mutans, Staphlococcus aureus, Salmonella enterica, Mycobacterium tuberculosis and others
Gene homologs encoding curli were recently determined also in four phyla: Bacteroidetes, Proteobacteria, Firmicutes, and Thermodesulfobacteria
changes in the gut microbiota induced by antibiotics alter neuroinflammation and amyloid deposition in a mouse model of AD
Our data suggest that amyloid proteins in the microbiota are involved in the origination and maintenance of neurodegenerative disease.
exposure to bacteria producing a functional extracellular amyloid protein enhances aggregation of AS in brain neurons in aged rats and in muscle cells in nematodes
AS aggregates seed aggregation of tau
involvement of the vagus nerve in PD
microgliosis, astrogliosis and enhanced expression of IL-6, TLR2 and TNF in the brain following curli exposure suggest the occurrence of an enhanced local sterile inflammatory response to AS in the brain.
the immune system in both AD and PD have now been extensively established
TLR2 activation through exposure to bacterial amyloid is pathogenic
Gut bacteria may play crucial role in systemic inflammation that leads to Alzheimer's and Parkinson's disease. These amyloid production bacteria trigger systemic inflammation that leads to microglia activation and amyloid in the brain. More establishment of the gut-brain connection.
Treg act to prevent spontaneous autoimmunity and to limit collateral damage to healthy tissues during adaptive immunity. However, these cells also have the potential to sabotage protective antimicrobial responses
Great T cell activiation review: Il-2 stimulates NK cells primarily release from TH1 cells and T cytotoxic lymphocytes are under the control of IL-12 released primarily from dendritic cells. Inflammatory cytokines in the presence of Treg to stimulate CD4+CD25- T cell activation.
The gut microbial composition is altered during pregnancy
probiotic supplements may contribute to the maintenance of bacterial diversity and glucose homeostasis in individuals with metabolic disturbances
Assessment of four randomized controlled trials in this review involving 288 pregnant women with GDM found that a 6–8 week probiotic intervention did not improve FBG or LDL-cholesterol levels
probiotic supplementation in women with GDM was associated with significant reductions in insulin resistance
One proposed method is by the production of short chain fatty acids (SCFAs), generated as a by-product of bacterial fermentation of dietary fibers. SCFAs act as an energy source for intestinal cells and have been found to regulate the production of hormones effecting energy intake and expenditure such as leptin and grehlin
Another hypothesized mechanism of SCFA action includes reducing gastrointestinal permeability by upregulating transcription of tight junction proteins, enhancing production of Glucagon-like peptide-2 (GLP-2) which promotes crypt cell proliferation, and reducing inflammation in colonic epithelial cells by increasing PPAR-gamma activation
Maintenance of the integrity of the gut barrier minimizes the concentration of lipopolysaccharide (LPS) in circulation
LPS is a structural component of gram negative bacterial cell walls, which induces an immune-cell response upon absorption into the human bloodstream, stimulating proinflammatory cytokine production and the onset of insulin resistance and hyperglycemia
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High fat and high calorie diets associated with increased colorectal cancer risk through alteration of gut flora. The exact mechanism between the altered gut flora and the cancer risk is unknown, per the authors, but the inflammation is likely the connection.