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10:33

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Helminth infection impairs autophagy-mediated killing of bacterial enteropathogens by macrophages

Chien-wen Su1, Yue Cao, Mei Zhang

  • 1Mucosal Immunology Laboratory, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|June 27, 2012
PubMed

Insights

Helminth infections impair macrophage autophagy, a key process for killing bacteria like Citrobacter rodentium. This suppression, mediated by IL-4 and IL-13, involves reduced LC3 protein, worsening bacterial infections.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Autophagy is crucial for macrophages to eliminate intracellular pathogens.
  • This study investigates autophagy's role in clearing extracellular bacteria, Citrobacter rodentium, post-phagocytosis.

Purpose of the Study:

  • To determine if helminth infection impacts macrophage autophagy of Citrobacter rodentium.
  • To elucidate the mechanisms behind helminth-induced modulation of autophagy.

Main Methods:

  • Macrophages from Heligmosomoides polygyrus-infected mice were analyzed for autophagy function.
  • STAT6-deficient mice were used to assess Th2 dependency.
  • Macrophages were treated with IL-4 and IL-13 to mimic helminth effects.
  • Expression and processing of LC3 (light chain 3) protein were quantified.
  • LC3 knockdown was performed to assess its role in bacterial killing.

Main Results:

  • Macrophage autophagy of Citrobacter rodentium was significantly impaired by H. polygyrus infection.
  • This impairment was Th2-dependent, involving STAT6 signaling and IL-4/IL-13.
  • Helminth infection decreased LC3 expression and processing in a STAT6-dependent manner.
  • LC3 knockdown confirmed its essential role in autophagic killing of Citrobacter.

Conclusions:

  • Helminth infection suppresses macrophage autophagy, contributing to increased susceptibility to bacterial pathogens.
  • The findings reveal a novel mechanism of helminth-induced immunosuppression impacting bacterial clearance.
  • This study provides mechanistic insight into how H. polygyrus exacerbates Citrobacter infections.

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