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Microscopy-based Assays for High-throughput Screening of Host Factors Involved in Brucella Infection of Hela Cells
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Cutting Edge: Brucella abortus exploits a cellular prion protein on intestinal M cells as an invasive receptor

Gaku Nakato1, Koji Hase, Michio Suzuki

  • 1Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, Kanagawa 230-0045, Japan;

Journal of Immunology (Baltimore, Md. : 1950)
|July 10, 2012
PubMed

Insights

Brucella abortus invades the gastrointestinal tract by entering microfold (M) cells, utilizing cellular prion protein (PrP(C)) as a key receptor. This finding clarifies the initial entry mechanism for oral brucellosis infections.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Brucella abortus is a Gram-negative bacterium responsible for brucellosis.
  • The specific entry site of orally ingested B. abortus in the gastrointestinal tract remains largely undefined.
  • Microfold cells (M cells) are specialized epithelial cells in the gut lining known for antigen sampling.

Purpose of the Study:

  • To elucidate the initial gastrointestinal entry site of orally administered Brucella abortus.
  • To investigate the role of microfold cells (M cells) in B. abortus infection.
  • To determine the involvement of cellular prion protein (PrP(C)) in the M cell uptake of B. abortus.

Main Methods:

  • In vitro and in vivo studies using wild-type and PrP(C)-deficient (Prnp(-/-)) mice.
  • Microscopy to observe the interaction between B. abortus, M cells, and PrP(C).
  • Oral infection models to assess bacterial translocation into Peyer's patches.

Main Results:

  • Brucella abortus was selectively internalized by M cells.
  • Colocalization of B. abortus and PrP(C) was observed on the apical surface and within M cells.
  • Internalization and translocation of B. abortus were significantly reduced in PrP(C)-deficient mice compared to wild-type mice.

Conclusions:

  • Orally ingested Brucella abortus invades the host primarily through M cells.
  • Cellular prion protein (PrP(C)) on the M cell apical surface acts as an uptake receptor for B. abortus.
  • This mechanism highlights a crucial step in the pathogenesis of oral brucellosis.

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