International Journal of Microbiology
Volume 2009 (2009), Article ID 753278, 11 pages
doi:10.1155/2009/753278
Research Article

Epithelial Cell Gene Expression Induced by Intracellular Staphylococcus aureus

Xianglu Li,1 William G. Fusco,1,2 Keun S. Seo,1 Kenneth W. Bayles,1,3 Erin E. Mosley,4 Mark A. McGuire,4 and Gregory A. Bohach1

1Department of Microbiology, Molecular Biology and Biochemistry, University of Idaho, Moscow, ID 83844, USA
2Environmental Biotechnology Institute, University of Idaho, Moscow, ID 83844, USA
3Department of Pathology & Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA
4Department of Animal and Veterinary Science (AVS), University of Idaho, Moscow, ID 83844, USA

Received 5 September 2008; Accepted 14 November 2008

Academic Editor: Michael M. Tunney

Copyright © 2009 Xianglu Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

HEp-2 cell monolayers were cocultured with intracellular Staphylococcus aureus, and changes in gene expression were profiled using DNA microarrays. Intracellular S. aureus affected genes involved in cellular stress responses, signal transduction, inflammation, apoptosis, fibrosis, and cholesterol biosynthesis. Transcription of stress response and signal transduction-related genes including atf3, sgk, map2k1, map2k3, arhb, and arhe was increased. In addition, elevated transcription of proinflammatory genes was observed for tnfa, il1b, il6, il8, cxcl1, ccl20, cox2, and pai1. Genes involved in proapoptosis and fibrosis were also affected at transcriptional level by intracellular S. aureus. Notably, intracellular S. aureus induced strong transcriptional down-regulation of several cholesterol biosynthesis genes. These results suggest that epithelial cells respond to intracellular S. aureus by inducing genes affecting immunity and in repairing damage caused by the organism, and are consistent with the possibility that the organism exploits an intracellular environment to subvert host immunity and promote colonization.