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Subversion of cellular autophagy by Anaplasma phagocytophilum

Hua Niu1, Mamoru Yamaguchi, Yasuko Rikihisa

  • 1Department of Veterinary Biosciences, The Ohio State University, Columbus, OH 43210, USA.

Cellular Microbiology
|November 6, 2007
PubMed

Insights

Anaplasma phagocytophilum evades host defenses by hijacking the autophagy pathway. This bacterium replicates within a unique compartment, resembling an early autophagosome, to avoid lysosomal destruction and promote its growth.

Area of Science:

  • Microbiology
  • Cell Biology
  • Immunology

Background:

  • Anaplasma phagocytophilum causes human granulocytic anaplasmosis.
  • It is an obligatory intracellular pathogen that replicates in a unique host cell compartment.
  • The bacterium avoids the endosomal-lysosomal pathway after host cell entry.

Purpose of the Study:

  • To investigate the nature of the replicative compartment of Anaplasma phagocytophilum.
  • To determine the role of autophagy in Anaplasma phagocytophilum infection.
  • To elucidate the mechanisms by which Anaplasma phagocytophilum establishes infection.

Main Methods:

  • Immunofluorescence microscopy to detect autophagosome markers (GFP-LC3, Beclin 1).
  • Analysis of LC3-II levels during infection.
  • Treatment with autophagy modulators (rapamycin, 3-methyladenine).

Main Results:

  • Anaplasma phagocytophilum replicative inclusions exhibit hallmarks of early autophagosomes, including a double-lipid bilayer membrane and colocalization with GFP-LC3 and Beclin 1.
  • Increased LC3-II levels and enhanced infection upon rapamycin stimulation were observed.
  • Inhibition of autophagy by 3-methyladenine arrested bacterial growth without affecting internalization.

Conclusions:

  • Anaplasma phagocytophilum subverts the host autophagy machinery to create a replicative niche.
  • The bacterium utilizes an early autophagosome-like compartment segregated from lysosomes for proliferation.
  • This strategy allows Anaplasma phagocytophilum to evade innate immune clearance and establish infection.

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