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Syk facilitates phagosome-lysosome fusion by regulating actin-remodeling in complement-mediated phagocytosis

Hiroyuki Tabata1, Hiroyuki Morita1, Hiroaki Kaji1

  • 1Division of Biochemistry, Faculty of Pharmaceutical Sciences, Himeji Dokkyo University, 7-2-1 Kami-ohno, Himeji, Hyogo, 670-8524, Japan.

Scientific Reports
|December 17, 2020
PubMed

Insights

Tyrosine kinase Syk is essential for host defense, enabling phagosome-lysosome fusion for pathogen clearance. Syk signaling regulates actin remodeling, preventing pathogen survival within macrophages.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Effective phagocytosis by macrophages is vital for host defense against pathogens.
  • Lysosomal fusion with phagosomes is critical for pathogen degradation, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate the mechanisms of phagosome-lysosome fusion during complement-mediated phagocytosis.
  • To elucidate the role of actin remodeling and tyrosine kinase Syk in this process.

Main Methods:

  • Utilized macrophage-like differentiated HL60 and Syk-knockout (Syk-KO) HL60 cells.
  • Performed phagosome tracking analysis and assessed phagosome acidification.
  • Investigated the effect of F-actin stabilizing agents.

Main Results:

  • Syk-KO cells exhibited impaired phagosome-lysosome fusion, leading to insufficient acidification and Candida albicans survival.
  • F-actin structures surrounding phagosomes were transiently lost but immediately reconstructed in Syk-KO cells.
  • F-actin stabilization mimicked the fusion impairment observed in Syk-KO cells.

Conclusions:

  • Tyrosine kinase Syk signaling is crucial for regulating actin remodeling during phagosome-lysosome fusion.
  • Syk facilitates the complete disappearance of F-actin, promoting lysosomal fusion and effective pathogen clearance.

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