Exclusion of actin-binding protein p57/coronin-1 from bacteria-containing phagosomes in macrophages infected with

Tsuyoshi Hayashi1, Masaki Miyake, Takashi Fukui

  • 1Laboratory of Microbiology and Immunology and the Global COE Program, University of Shizuoka School of Pharmaceutical Sciences, 52-1 Yada, Suruga-ku, Shizuoka, Shizuoka 422-8526, Japan.

Insights

Coronin-1 (p57) is involved in the actin-dependent uptake of Legionella pneumophila into macrophages. This protein is excluded from phagosomes containing live Legionella, suggesting distinct entry pathways for this pathogen.

Area of Science:

  • Cell Biology
  • Microbiology
  • Immunology

Background:

  • Legionella pneumophila causes Legionnaires' disease by multiplying within human macrophages.
  • The pathogen evades host defenses within specialized phagosomes through poorly understood mechanisms.
  • Actin-binding proteins play crucial roles in phagocytosis and pathogen entry.

Purpose of the Study:

  • To investigate the role of the actin-binding protein p57/coronin-1 during Legionella infection.
  • To determine the localization and function of p57/coronin-1 during L. pneumophila uptake and intracellular trafficking.

Main Methods:

  • Fluorescence microscopy to observe co-localization of p57/coronin-1 and F-actin.
  • Treatment with cytochalasin D to assess the role of actin polymerization.
  • Analysis of p57/coronin-1 localization on phagosomes containing live or heat-killed L. pneumophila and opsonized zymosan.

Main Results:

  • p57/coronin-1 and F-actin co-localized at the plasma membrane during L. pneumophila adherence.
  • p57/coronin-1 localization was dependent on actin polymerization, indicating its role in bacterial uptake.
  • p57/coronin-1 was excluded from phagosomes containing live L. pneumophila and Legionella gratiana, but transiently associated with phagosomes containing opsonized zymosan or heat-killed bacteria.

Conclusions:

  • p57/coronin-1 is involved in the actin-dependent entry of L. pneumophila into macrophages.
  • Live Legionella species utilize distinct endocytic pathways that exclude p57/coronin-1, differentiating them from general phagocytic pathways leading to lysosomal degradation.

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