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The β2 Integrin Mac-1 Induces Protective LC3-Associated Phagocytosis of Listeria monocytogenes

Alexander Gluschko1, Marc Herb1, Katja Wiegmann1

  • 1Institute for Medical Microbiology, Immunology and Hygiene, University of Cologne, Cologne, Germany.

Cell Host & Microbe
|March 16, 2018
PubMed

Insights

LC3-associated phagocytosis (LAP) targets Listeria monocytogenes (L.m.) in macrophages, enhancing immunity. This pathway, initiated by Mac-1 and Nox2, is crucial for anti-L.m. defense in mice.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • The role of autophagy in controlling intracellular pathogens like Listeria monocytogenes (L.m.) is not fully understood.
  • Existing knowledge gaps regarding the specific mechanisms and immune consequences of L.m. targeting by cellular machinery.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which macrophages internalize and eliminate L.m.
  • To investigate the role of LC3-associated phagocytosis (LAP) in anti-Listerial immunity.

Main Methods:

  • In vivo studies using L.m. infection in macrophages.
  • Analysis of LC3-associated phagocytosis (LAP) and canonical autophagy pathways.
  • Investigating the roles of Mac-1, acid sphingomyelinase, and Nox2 in L.m. targeting.

Main Results:

  • L.m. infection exclusively induces LAP, not canonical autophagy, in macrophages.
  • LAP targeting of L.m. is essential for effective anti-Listerial immunity.
  • The Mac-1 receptor initiates a signaling cascade involving acid sphingomyelinase and Nox2, leading to LC3 recruitment and enhanced phagosome-lysosome fusion.

Conclusions:

  • LAP is a critical pathway for macrophage-mediated immunity against L.m.
  • Targeting L.m. via LAP enhances bacterial killing and improves host defense.
  • Understanding the Mac-1/Nox2/LAP axis provides insights into novel strategies for infectious disease control.
Keywords:
LC3-associated phagocytosisListeria monocytogenesMac-1/CR3NAPDH oxidase Nox2ROSacid sphingomyelinaselysosomemacrophagesnon-canonical autophagyβ(2) integrin

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