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Inhibition of macrophage autophagy induced by Salmonella enterica serovar typhi plasmid

ShuYan Wu1, YuanYuan Chu1, YanRu Yang1

  • 1Medical College of Soochow University, No. 199, Ren Ai Road, Suzhou, Jiangsu 215123, P. R. China.

Frontiers in Bioscience (Landmark Edition)
|January 7, 2014
PubMed

Insights

The Salmonella plasmid pR(ST98) hinders macrophage autophagy and promotes apoptosis, enhancing bacterial survival and proliferation during infection. This plasmid plays a key role in Salmonella pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Molecular Biology

Background:

  • Salmonella enterica serovar typhi (S. typhi) harbors the chimeric plasmid pR(ST98), implicated in multidrug resistance and virulence.
  • The precise role of pR(ST98) in bacterial pathogenesis, particularly its interaction with host immune cells, remains incompletely understood.

Purpose of the Study:

  • To investigate the role of the pR(ST98) plasmid in modulating macrophage autophagy and apoptosis during S. typhi infection.
  • To determine the impact of pR(ST98) on intracellular bacterial survival and proliferation.

Main Methods:

  • Murine macrophage-like cell line (J774A.1) infection models using S. typhi wild-type, pR(ST98) deletion mutant, and complemented strains.
  • Assessment of autophagy vacuoles, expression of autophagy markers (Beclin 1, LC3-II), and macrophage apoptosis rates.
  • Evaluation of intracellular bacterial survival and proliferation.
  • Intervention with the autophagy agonist rapamycin.

Main Results:

  • S. typhi harboring pR(ST98) reduced macrophage autophagy vacuoles and the expression of Beclin 1 and LC3-II.
  • Macrophages infected with the pR(ST98) deletion mutant exhibited lower apoptosis rates compared to wild-type or complemented strains.
  • Intracellular bacteria carrying pR(ST98) demonstrated significantly higher survival rates.
  • Rapamycin treatment decreased apoptosis and intracellular bacterial growth in cells infected with S. typhi containing pR(ST98).

Conclusions:

  • The pR(ST98) plasmid inhibits host macrophage autophagy.
  • pR(ST98) induces macrophage apoptosis, facilitating bacterial survival and proliferation within the host.
  • This plasmid contributes significantly to Salmonella pathogenesis by manipulating host immune responses.

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