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Updated: Jun 24, 2026

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
07:10

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

Early gene expression changes induced by the bacterial superantigen staphylococcal enterotoxin B and its modulation

Govindarajan Rajagopalan1, Ashenafi Y Tilahun, Yan W Asmann

  • 1Department of Immunology, Mayo Clinic College of Medicine, Rochester, Minnesota 55905, USA. rajagopalan.govindarajan@mayo.edu

Physiological Genomics
|April 2, 2009
PubMed

Insights

Toxic shock syndrome (TSS) involves complex molecular events. This study used a transgenic mouse model to identify early inflammatory responses and potential therapeutic targets like bortezomib for superantigen-induced TSS.

Area of Science:

  • Immunology
  • Molecular Biology
  • Microbiology

Background:

  • Toxic shock syndrome (TSS) is a severe systemic illness caused by bacterial superantigens.
  • Understanding TSS pathogenesis has been limited by the lack of suitable animal models.
  • Early molecular events in TSS require detailed characterization to identify therapeutic targets.

Purpose of the Study:

  • To characterize early molecular events in toxic shock syndrome pathogenesis.
  • To investigate the efficacy of bortezomib in modulating superantigen-induced gene expression in a mouse model.

Main Methods:

  • Utilized a human leukocyte antigen (HLA)-DR3 transgenic mouse model for TSS studies.
  • Employed DNA microarrays for gene expression profiling after staphylococcal enterotoxin B (SEB) administration.
  • Analyzed serum cytokine and chemokine levels and pathway modulation.
  • Assessed the effect of bortezomib on SEB-induced gene expression.

Main Results:

  • Identified rapid upregulation of pro- and anti-inflammatory mediators, including Th0, Th1, Th2, and Th17 cytokines, immunoregulatory cytokines, chemokines, and proteases.
  • Observed significant elevation in serum levels of several identified cytokines and chemokines.
  • Pathway analysis revealed significant modulation of biochemical and cellular functions.
  • Bortezomib treatment significantly modulated SEB-induced gene expression, indicating potential therapeutic benefit.

Conclusions:

  • Toxic shock syndrome is a complex inflammatory process with a distinct early molecular signature.
  • The HLA-DR3 transgenic mouse model is valuable for studying TSS pathogenesis.
  • Bortezomib shows potential as a therapeutic agent for superantigen-induced TSS by modulating key inflammatory pathways.

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