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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

STING/MPYS mediates host defense against Listeria monocytogenes infection by regulating Ly6C(hi) monocyte migration

Lei Jin1, Andrew Getahun, Heather M Knowles

  • 1Integrated Department of Immunology, University of Colorado Denver School of Medicine and National Jewish Health, Denver, CO 80206, USA. jinl@mail.amc.edu

Journal of Immunology (Baltimore, Md. : 1950)
|February 5, 2013
PubMed

Insights

MPYS (Mediator of DNA sensing and IFN-γ production) protein is crucial for controlling bacterial infections, particularly Listeria monocytogenes, by regulating monocyte migration and function.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • MPYS (also known as STING, MITA, and TMEM173) is a key mediator of type I IFN production, vital for antiviral immunity.
  • Its role in host defense against bacterial pathogens in vivo remains largely unexplored.

Purpose of the Study:

  • To investigate the in vivo function of MPYS in host defense against bacterial infection, specifically Listeria monocytogenes.
  • To elucidate the mechanisms underlying MPYS-mediated immunity against nonviral pathogens.

Main Methods:

  • Utilized MPYS-deficient (Tmem173()) and wild-type mice for Listeria monocytogenes infection models.
  • Analyzed chemokine production (MCP-1, MCP-3) and monocyte populations (Ly6C(hi)) in blood and liver.
  • Performed adoptive transfer of wild-type Ly6C(hi) monocytes into MPYS-deficient mice.

Main Results:

  • MPYS deficiency led to increased bacterial burden in the liver following Listeria monocytogenes infection.
  • This increase was associated with reduced MCP-1 and MCP-3 chemokine levels and lower Ly6C(hi) monocyte frequency.
  • MPYS-deficient Ly6C(hi) monocytes exhibited impaired migration to the liver.
  • Adoptive transfer of wild-type Ly6C(hi) monocytes ameliorated the increased bacterial load in MPYS-deficient mice.

Conclusions:

  • MPYS plays a critical, type I IFN-independent role in host defense against Listeria monocytogenes infection.
  • MPYS regulates Ly6C(hi) monocyte recruitment and function, crucial for controlling bacterial dissemination in the liver.
  • This study uncovers a novel mechanism of MPYS in innate immunity against bacterial pathogens.

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