Reprogramming of Cell Death Pathways by Bacterial Effectors as a Widespread Virulence Strategy

Joseph J. Wanford, Abderrahman Hachani*, Charlotte Odendall

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

11 Citations (Scopus)

Abstract

The modulation of programmed cell death (PCD) processes during bacterial infections is an evolving arms race between pathogens and their hosts. The initiation of apoptosis, necroptosis, and pyroptosis pathways are essential to immunity against many intracellular and extracellular bacteria. These cellular self-destructive mechanisms are used by the infected host to restrict and eliminate bacterial pathogens. Without a tight regulatory control, host cell death can become a double-edged sword. Inflammatory PCDs contribute to an effective immune response against pathogens, but unregulated inflammation aggravates the damage caused by bacterial infections. Thus, fine-tuning of these pathways is required to resolve infection while preserving the host immune homeostasis. In turn, bacterial pathogens have evolved secreted virulence factors or effector proteins that manipulate PCD pathways to promote infection. In this review, we discuss the importance of controlled cell death in immunity to bacterial infection. We also detail the mechanisms employed by type 3 secreted bacterial effectors to bypass these pathways and their importance in bacterial pathogenesis.

Original languageEnglish
JournalInfection and Immunity
Volume90
Issue number5
DOIs
Publication statusPublished - May 2022

Keywords

  • apoptosis
  • immunity
  • infection
  • inflammasome
  • inflammation
  • necroptosis
  • programmed cell death
  • pyroptosis
  • T3SS
  • virulence

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