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Evaluating Shigella flexneri Pathogenesis in the Human Enteroid Model.

Sridevi Ranganathan1, Michele Doucet2, Christen L Grassel1

  • 1Center for Vaccine Development and Global Health, University of Maryland School of Medicine, Baltimore, Maryland, USA.

Infection and Immunity
|January 16, 2019
PubMed
Summary
This summary is machine-generated.

Shigella flexneri infects human intestinal enteroids, a more accurate model of the gut. This research highlights the enteroid model

Keywords:
M cellsS. flexneri pathogenesiscolonoidhuman intestinal enteroids

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Area of Science:

  • Microbiology
  • Gastroenterology
  • Infectious Diseases

Background:

  • Shigella is a major cause of childhood diarrhea and death globally.
  • Existing cell lines and animal models poorly represent human Shigella infection.
  • The human intestinal enteroid model offers a more physiologically relevant system.

Purpose of the Study:

  • To evaluate the human intestinal enteroid model for studying Shigella pathogenesis.
  • To investigate Shigella flexneri infection dynamics within enteroids.
  • To assess host responses to Shigella infection in the enteroid model.

Main Methods:

  • Utilized human intestinal enteroids derived from LGR5+ stem cells.
  • Inoculated enteroids with Shigella flexneri via apical and basolateral surfaces.
  • Quantified bacterial invasion and replication.
  • Measured host responses including cytokine secretion and mucin expression.

Main Results:

  • Shigella flexneri infected and replicated within human enteroids from various intestinal segments.
  • Apical invasion was limited but increased significantly with M cell differentiation.
  • Basolateral invasion was substantially more efficient than apical invasion.
  • Infection induced increased interleukin-8 secretion and Muc2 expression.

Conclusions:

  • Human intestinal enteroids serve as a valuable model for studying Shigella pathogenesis.
  • Enteroids provide a more accurate representation of host-pathogen interactions than traditional models.
  • This model bridges the gap between in vitro, animal, and human infection studies.