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Flow Cytometric Measurement Of ROS Production In Macrophages In Response To FcγR Cross-linking
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Mucosal reactive oxygen species decrease virulence by disrupting Campylobacter jejuni phosphotyrosine signaling

Nicolae Corcionivoschi1, Luis A J Alvarez, Thomas H Sharp

  • 1National Children's Research Centre, Our Lady's Children's Hospital Crumlin, Dublin, Ireland.

Cell Host & Microbe
|July 24, 2012
PubMed

Insights

Epithelial reactive oxygen species (ROS) generated during Campylobacter jejuni infection disrupt bacterial signaling pathways, impairing capsule formation and reducing pathogen virulence. This highlights a novel host defense mechanism against bacterial infections.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Reactive oxygen species (ROS) are crucial for mucosal defense, but their induction and impact on pathogens remain incompletely understood.
  • Campylobacter jejuni is a significant foodborne pathogen, and its virulence factors are key targets for therapeutic intervention.

Purpose of the Study:

  • To investigate the role of epithelial NADPH oxidases in generating ROS during C. jejuni infection.
  • To elucidate the mechanisms by which ROS affect C. jejuni capsule formation and virulence.
  • To identify the specific bacterial signaling pathways targeted by ROS.

Main Methods:

  • Infection models of C. jejuni with epithelial cells.
  • Analysis of ROS production by epithelial NADPH oxidases (Nox1/Duox2).
  • Assessment of bacterial capsule formation, virulence, and signal transduction pathways, including protein phosphorylation.

Main Results:

  • Epithelial NADPH oxidases generate ROS upon C. jejuni invasion.
  • ROS inhibit the bacterial phosphotyrosine network by inactivating the Cjtk tyrosine kinase.
  • ROS-mediated Cjtk inactivation reduces phosphorylation of key enzymes like Gne, impairing capsule synthesis and virulence.

Conclusions:

  • Epithelial NADPH oxidases serve as an early antibacterial defense mechanism in the intestinal mucosa.
  • ROS disrupt C. jejuni virulence by altering bacterial signal transduction and capsule formation.
  • Targeting epithelial ROS production or bacterial signaling pathways could offer new therapeutic strategies against C. jejuni infections.

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