Microbiome & Chronic Diseases

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Fusobacterium nucleatum ⇒ Fusobacterium {10000137}

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Fusobacterium nucleatum


Initialisation date:


Meta Information

Enzyme:[  ]
Cancerogenic, Pro-inflamatory


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References Notes

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Shared Reference Notes

  • [1.30
    - F. nucleatum and certain co-occurring bacteria were present not only in primary tumors but also in distant metastases. Preliminary evidence suggests that the bacterium is localized primarily within the metastatic #Cancer cells rather than in the stroma. - Antibiotic treatment of mice carrying xenografts of F. nucleatum–positive human colorectal #Cancer slowed tumor growth, consistent with a causal role for the bacterium in tumorigenesis.
  • [1.31] [#Colorectal cancer
    - Chronic inflammation is an established risk factor for CRC, as patients with inflammatory bowel diseases (IBD) consistently have a higher risk than the general population of developing CRC. - An increase in pro-inflammatory species has been repeatedly reported in CRC patients. - The most prevalent and most described bacterium in CRC fecal and mucosa-associated microbiota is Fusobacterium nucleatum
  • [1.7] [#Colorectal cancer
    - Fusobacterium nucleatum expresses adhesins, including FadA and Fap2, which bind to tumour cells and directly promote carcinogenesis by activating oncogenic Wnt/β-catenin signalling and dysregulating immune cell infiltration and antitumour immunity.
  • [1.33
    - The direct bond of microbial proteins with E-cadherin of host epithelial cells can activate the β-catenin pathway, as expressed by Fusobacterium nucleatum, associated with #Colorectal cancer. - F. nucleatum, expressing Fap2 cell surface protein, inhibits immune cytotoxicity through interaction with T and NK cells
  • [1.34] [#Colorectal cancer
    - CRC mouse model > Oral microbiota alterations change > the gut bacterial composition within tumors but not in adjacent peritumor tissues. - Buccal Fusobacterium nucleatum migrates > to the CRC locus > impairs the therapeutic efficacy and prognosis of #Radiotherapy. Administration of a specific antibiotic, metronidazole > abrogates the adverse effects of oral microbiome fluctuation on #Radiotherapy for CRC.
  • [1.35] [#Colorectal cancer
    - Increases in #Enterococcus faecalis and #Escherichia coli enhance the production of intestinal inflammatory signaling molecules, IFN-γ and IL-4. In both IBD and CRC, Fusobacterium nucleatum elicits strong pro-inflammatory responses
  • [#Alzheimer’s disease] [#Amyloid-beta, #Lipopolysaccharide] - antibodies to F. nucleatum can be detected in the serum of patients with AD or cognitive impairment. - F. nucleatum activates microglial cells causing morphological changes, accelerated proliferation and enhanced expression of TNF-α and IL-1β in microglial cells. - LPS promoted the proliferation of brain microglia - F. nucleatum-induced periodontitis resulted in the exacerbation of Alzheimer’s symptoms in 5XFAD mice including increased cognitive impairment, beta-amyloid accumulation and Tau protein phosphorylation in the mouse cerebrum. - The stimnuli like LPS, Aβ or IFN-γ would activate microglial M1 phenotype, leading to the expression of pro-inflammatory cytokines and irreversible neuron loss. - The main known virulence factors of F. nucleatum include FadA, Fap2, and LPS
  • [1.36] [#Hepatocellular cancer
    - Fusobacterium nucleatum was found to directly interact with TIGIT through the FAP2 protein, with subsequent inhibition of NK cells which have significant anti-tumor properties
  • [1.37] [#Cancer
    - F. nucleatum subdue host immune response and triggers cellular proliferation.
  • [1.38] [#Alzheimer’s disease] [#Amyloid-beta
    - Fusobacterium nucleatum can increased TNF-α and IL-1β expression in microglial cells, and also in vivo it can increase cognitive impairment, beta-amyloid accumulation and Tau protein phosphorylation in the cerebrum of an AD animal model.

Common References