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Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes
12:50

Measuring Bacterial Load and Immune Responses in Mice Infected with Listeria monocytogenes

Published on: August 9, 2011

Listeria monocytogenes induces apoptosis of infected hepatocytes

H W Rogers1, M P Callery, B Deck

  • 1Center for Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|January 15, 1996
PubMed

Insights

Listeria monocytogenes infection causes liver cell death (apoptosis) and inflammation, forming microabscesses. Infected liver cells trigger immune responses independently of cytokine signaling.

Area of Science:

  • Hepatology
  • Infectious Diseases
  • Immunology

Background:

  • Blood-borne Listeria monocytogenes preferentially infects liver cells (hepatocytes).
  • Listeria infection leads to the formation of liver microabscesses and hepatocyte apoptosis.

Purpose of the Study:

  • To investigate the role of hepatocyte apoptosis in Listeria infection.
  • To understand the inflammatory response initiated by infected hepatocytes.

Main Methods:

  • Infection of cultured hepatocytes with Listeria monocytogenes.
  • Observation of hepatocyte apoptosis and neutrophil chemoattractant release.
  • Assessment of cytokine effects on bacterial multiplication and cell death.

Main Results:

  • Hepatocyte apoptosis occurs at the microabscess edge and is evident even with neutrophil depletion.
  • Infected hepatocytes undergo apoptosis, releasing neutrophil chemoattractants.
  • Cytokines do not inhibit Listeria multiplication within cultured hepatocytes.

Conclusions:

  • Hepatocytes initiate an early inflammatory program upon Listeria infection.
  • This cellular response, including apoptosis and chemoattractant release, is independent of external cytokine signaling.

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