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Fusobacterium nucleatum Secretes Outer Membrane Vesicles and Promotes Intestinal Inflammation.

Melinda A Engevik1,2, Heather A Danhof3, Wenly Ruan4

  • 1Department of Pathology and Immunology, Baylor College of Medicine, Houston, Texas, USA melinda.engevik@bcm.edu.

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|March 3, 2021
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Summary

Fusobacterium nucleatum outer membrane vesicles activate Toll-like receptor 4 (TLR4) and NF-κB signaling, promoting intestinal inflammation. This effect is dependent on antibiotic-induced alterations in the gut microbiome.

Keywords:
Fusobacterium nucleatumTLR4enteroidsepitheliuminflammationintestinemicrobiomeorganoidsouter membrane vesicles

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Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Microbes are implicated in inflammation, but mechanisms are unclear.
  • Fusobacterium species are found in the gut mucosa of patients with digestive diseases.
  • The role of Fusobacterium nucleatum in promoting intestinal inflammation requires elucidation.

Purpose of the Study:

  • To investigate the role of Fusobacterium nucleatum in promoting intestinal inflammation.
  • To identify the specific components of F. nucleatum responsible for stimulating inflammatory responses.
  • To elucidate the signaling pathways involved in F. nucleatum-induced inflammation.

Main Methods:

  • Exposure of colonic epithelial cells and human colonoid monolayers to F. nucleatum conditioned media and purified outer membrane vesicles (OMVs).
  • Pharmacological inhibition of Toll-like receptor 4 (TLR4) and assessment of downstream signaling pathways (p-ERK, p-CREB, NF-κB).
  • In vivo studies using mice with human microbiota, involving antibiotic pretreatment and F. nucleatum gavage, followed by histological and gene expression analysis.

Main Results:

  • F. nucleatum OMVs (>50 kDa) stimulated interleukin-8 (IL-8) and tumor necrosis factor (TNF) production via TLR4 activation.
  • F. nucleatum components activated downstream signaling molecules p-ERK, p-CREB, and NF-κB in vitro.
  • In vivo, F. nucleatum induced colonic inflammation, architectural disruption, immune cell infiltration, and increased pro-inflammatory cytokine expression, contingent on antibiotic-induced microbiome alterations.

Conclusions:

  • F. nucleatum, particularly its OMVs, promotes pro-inflammatory signaling cascades.
  • Activation of TLR4 and NF-κB pathways by F. nucleatum contributes to intestinal inflammation.
  • The pro-inflammatory effects of F. nucleatum are dependent on alterations in the gut microbiome, suggesting a context-specific role in disease pathogenesis.