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High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages
11:10

High-throughput Assay to Phenotype Salmonella enterica Typhimurium Association, Invasion, and Replication in Macrophages

Published on: August 11, 2014

Penetration and activation of brain endothelium by Salmonella enterica serovar Typhimurium

Nina M van Sorge1, Patricia A Zialcita, Sara H Browne

  • 1Department of Pediatrics, University of California, San Diego, La Jolla, USA.

The Journal of Infectious Diseases
|December 28, 2010
PubMed

Insights

Salmonella Typhimurium invades the human blood-brain barrier by rearranging host cell structures, not requiring a specific secretion system. This invasion triggers an immune response, potentially leading to Salmonella meningitis.

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Microbiology

Background:

  • Salmonella meningitis is a severe central nervous system infection, prevalent in Africa.
  • The blood-brain barrier (BBB) protects the brain from pathogens.

Purpose of the Study:

  • To investigate the mechanisms of Salmonella enterica serovar Typhimurium adherence, invasion, and penetration of the human BBB.
  • To understand the host immune response during Salmonella infection of brain microvascular endothelial cells.

Main Methods:

  • Utilized human brain microvascular endothelial cells (hBMECs) to model the BBB.
  • Observed Salmonella Typhimurium interactions with hBMECs.
  • Assessed the role of host actin cytoskeleton and type III secretion system in invasion.
  • Analyzed the immune response, including neutrophil signaling and recruitment.

Main Results:

  • Salmonella Typhimurium adhered to, invaded, and penetrated hBMECs.
  • Invasion depended on host actin cytoskeleton rearrangements.
  • A functional type III secretion system was not essential for invasion.
  • Salmonella infection induced a proinflammatory immune response impacting neutrophil activity.

Conclusions:

  • Salmonella Typhimurium can breach the human BBB by exploiting host cell mechanisms.
  • Host actin rearrangement is critical for Salmonella invasion of brain endothelial cells.
  • The induced immune response may contribute to BBB penetration and meningitis development.

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