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Fusobacterium nucleatum ⇒ Fusobacterium {10000137}

Record Keys


Organism:
Fusobacterium nucleatum
Parent:

Details


Initialisation date:
2019-09-01

Links


Meta Information


Rank:
Species
Domain:
Bacteria
Zone:
Gut
Oronasal
Enzyme:[  ]
Function:
Cancerogenic, Pro-inflamatory

Notes:


[  ]

References Notes


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Shared Reference Notes


  • [1.29
    - 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.
  • [1.30
    - 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
    - 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.
  • [1.32
    - 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
  • [1.33
    - 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.
  • [1.34
    - 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
  • - 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
  • [1.35
    - 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

Common References