Differential responses of macrophages to Salmonella enterica serovars Enteritidis and Typhimurium

Masashi Okamura1, Hyun S Lillehoj, Richard B Raybourne

  • 1Animal Parasitic Diseases Laboratory, Animal and Natural Resources Institute, Agricultural Research Service, US Department of Agriculture, Bldg 1040 BARC-East Beltsville, MD 20705, USA.

Insights

Chicken macrophages show different responses to Salmonella Enteritidis (SE) and Salmonella Typhimurium (ST). ST infection leads to increased macrophage death and inflammation compared to SE, influencing Salmonella

Area of Science:

  • Immunology
  • Microbiology
  • Veterinary Science

Background:

  • Macrophages are key immune cells involved in Salmonella infection, controlling bacterial replication and spreading.
  • Differential interactions between host macrophages and Salmonella serovars may influence disease pathogenesis and host specificity.

Purpose of the Study:

  • To investigate the distinct responses of chicken macrophages to Salmonella enterica serovar Enteritidis (SE) and serovar Typhimurium (ST).
  • To determine the role of macrophage phagocytosis, intracellular bacterial viability, and nitric oxide (NO) production in differential responses to SE and ST.

Main Methods:

  • In vitro infection of chicken macrophages with SE and ST, with and without interferon-gamma (IFN-gamma).
  • Assessment of bacterial phagocytosis, intracellular viability, and nitric oxide production.
  • Evaluation of the effects of bacterial components (LPS, OMP, flagella) on macrophage NO production.

Main Results:

  • Macrophage phagocytosis rates for SE and ST were similar, with or without IFN-gamma.
  • Intracellular viable SE were significantly reduced compared to ST, irrespective of IFN-gamma presence.
  • Salmonella infection synergized with IFN-gamma to induce nitric oxide production.
  • ST infection, particularly with IFN-gamma, induced increased macrophage necrosis and NO production compared to SE.

Conclusions:

  • Chicken macrophage responses differ significantly between SE and ST infections.
  • ST infection may lead to increased macrophage death and a heightened inflammatory response compared to SE.
  • These differential immune responses could contribute to the distinct disease tropisms observed between SE and ST.