Jul 24, 2012

Infection-induced host translational blockage inhibits immune responses and epithelial renewal in the Drosophila gut

Cell Host & Microbe
Sveta ChakrabartiBruno Lemaitre

Abstract

Typically, immune responses control the pathogen, while repair and stress pathways limit damage caused by pathogenesis. The relative contribution of damage to the outcome of pathogenesis and the mechanistic links between the immune and repair pathways are poorly understood. Here, we analyze how the entomopathogenic bacterium Pseudomonas entomophila induces irreversible damage to the Drosophila gut. We find that P. entomophila ingestion induces a global translational blockage that impairs both immune and repair programs in the fly gut. P. entomophila-induced translational inhibition is dependent on bacterial pore forming toxins and reactive oxygen species produced by the host in response to infection. Translational arrest is mediated through activation of the GCN2 kinase and inhibition of the TOR pathway as a consequence of host damage. Together, our study draws a model of pathogenesis in which bacterial inhibition of translation by excessive activation of stress responsive pathways inhibits both immune and regenerative epithelial responses.

  • References33
  • Citations63

References

Mentioned in this Paper

Pseudomonas Infections
Immune Response
Trimethylamine-N-oxide Reductase (Cytochrome C) Activity
Pathogenic Aspects
Biochemical Pathway
Microarray Analysis
Galactosidase Activity
Fat Pad
Pseudomonas entomophila
Heat-Shock Proteins 70

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