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Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages
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Isolation of Salmonella typhimurium-containing Phagosomes from Macrophages

Published on: October 25, 2017

The late endosomal adaptor p14 is a macrophage host-defense factor against Salmonella infection

Nicole Taub1, Manfred Nairz, Diana Hilber

  • 1Biocenter, Division of Cell Biology, Innsbruck Medical University, Innsbruck 6020, Austria.

Journal of Cell Science
|March 20, 2012
PubMed

Insights

The protein p14 (also known as LAMTOR2) is crucial for cellular defense against Salmonella Typhimurium infection. It ensures timely endosomal transport, preventing bacterial replication and aiding host survival.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Host-pathogen interactions are determined by the interplay between host resistance and bacterial virulence.
  • Intracellular pathogens like Salmonella Typhimurium pose significant challenges to host defense mechanisms.
  • The endolysosomal system plays a critical role in cellular immunity and pathogen trafficking.

Purpose of the Study:

  • To investigate the role of the late endosomal adaptor p14 (LAMTOR2) in host defense against Salmonella Typhimurium.
  • To elucidate the mechanism by which p14 influences Salmonella trafficking and replication within host cells.
  • To determine the in vivo significance of p14 in combating Salmonella infection.

Main Methods:

  • Utilized cell culture models (professional phagocytes and non-phagocytic cells) to study Salmonella infection.
  • Employed techniques to assess the impact of p14 deficiency on bacterial intracellular transport.
  • Investigated the activation of antimicrobial effector systems (NADPH oxidase, iNOS) in the presence or absence of p14.
  • Conducted in vivo studies using mouse models to evaluate the role of p14 in Salmonella infection outcome.

Main Results:

  • Loss of p14 disrupts the timely transport of Salmonella through the endolysosomal system.
  • p14 deficiency creates a window allowing Salmonella to enter a replication niche.
  • Absence of p14 leads to inappropriate activation of antimicrobial systems like NADPH oxidase and inducible nitric oxide synthase.
  • p14-deficient cells show increased Salmonella replication both in professional phagocytes and non-phagocytic cells.
  • Mice lacking p14 exhibit impaired ability to control Salmonella infection.

Conclusions:

  • p14 is an essential host factor for cellular defense against Salmonella Typhimurium.
  • p14 facilitates accurate Salmonella transport within the endolysosomal pathway, limiting bacterial replication.
  • p14's function is critical for both in vitro and in vivo control of Salmonella infection, highlighting its importance in host immunity.

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