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Role of the type 6 secretion system on apoptosis and macrophage polarization during Burkholderia pseudomallei

Jacob L Stockton1, Nittaya Khakhum1, Alfredo G Torres1,2

  • 1Department of Microbiology and Immunology, University of Texas Medical Branch Galveston, Texas, United States of America.

Plos Neglected Tropical Diseases
|October 15, 2024
PubMed

Insights

The Burkholderia pseudomallei type 6 secretion system (T6SS) exacerbates apoptotic cell death and lung inflammation during melioidosis infection. M2 macrophage polarization aids bacterial replication, highlighting T6SS

Area of Science:

  • Bacteriology and Immunology
  • Pathogen-Host Interactions

Background:

  • Burkholderia pseudomallei (Bpm) causes melioidosis, a disease characterized by intracellular bacterial replication.
  • The Bpm type 6 secretion system (T6SS) is a key virulence factor involved in multinucleated giant cell (MNGC) formation and bacterial spread.

Purpose of the Study:

  • To investigate the role of T6SS in modulating host cell death, macrophage polarization, and lung inflammation during Bpm infection.
  • To elucidate the impact of T6SS on Bpm pathogenesis in macrophage and pulmonary infection models.

Main Methods:

  • Infection of macrophages and mice with Bpm strains exhibiting T6SS activity.
  • Assessment of apoptotic cell death, macrophage polarization markers (M1/M2), and lung histopathology.

Main Results:

  • T6SS significantly exacerbates apoptotic cell death in infected macrophages and lung tissues.
  • T6SS does not alter macrophage polarization but M2 polarization is found to be beneficial for Bpm replication.
  • T6SS contributes to increased severity of inflammatory nodule formation in the lungs, potentially linked to apoptosis.

Conclusions:

  • The T6SS is a critical determinant of host cell apoptosis and lung pathology during melioidosis.
  • M2 macrophage polarization may represent a pro-Bpm host environment, facilitating bacterial pathogenesis.
  • T6SS-induced apoptosis correlates with inflammatory responses in the lungs, suggesting a complex interplay between bacterial virulence and host immunity.

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