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Intracellular destruction of salmonellae in genetically resistant mice

F R Lin1, H S Hsu, V R Mumaw

  • 1Department of Microbiology and Immunology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.

Insights

Infection-resistant mice show immune cells actively destroying Salmonella typhimurium. Despite this, the bacteria proliferate extracellularly in the peritoneal cavity.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Salmonella typhimurium is a significant bacterial pathogen.
  • Inbred male A/J mice are genetically resistant to Salmonella infection.
  • Understanding the host-pathogen interaction in resistant models is crucial for immunology research.

Purpose of the Study:

  • To investigate the cellular response to Salmonella typhimurium infection in genetically resistant mice.
  • To examine the phagocytic and digestive capabilities of peritoneal exudate cells.
  • To observe the in vivo behavior and proliferation of Salmonella typhimurium.

Main Methods:

  • Intraperitoneal injection of virulent Salmonella typhimurium (2000 LD50) into A/J mice.
  • Harvesting of peritoneal exudate cells at various time points (5-54 h post-infection).
  • Examination of cells and bacteria using electron microscopy.

Main Results:

  • Polymorphonuclear leukocytes (PMNs) were observed actively ingesting and digesting Salmonella typhimurium as early as 5 hours post-infection.
  • Macrophages demonstrated sustained activity in phagocytosing and destroying the bacteria throughout the observation period.
  • Evidence of extracellular bacterial division, indicating proliferation within the peritoneal cavity, was observed.

Conclusions:

  • Genetically resistant mice mount a robust phagocytic response against Salmonella typhimurium via PMNs and macrophages.
  • Despite effective phagocytosis, Salmonella typhimurium can proliferate extracellularly in the peritoneal cavity of resistant hosts.
  • This study highlights a complex interplay between host resistance mechanisms and bacterial survival strategies.

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