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Mediators of Inflammation
Volume 2011, Article ID 971502, 8 pages
Research Article

Infection of Human Coronary Artery Endothelial Cells by Group B Streptococcus Contributes to Dysregulation of Apoptosis, Hemostasis, and Innate Immune Responses

1Institute of Clinical Biochemistry and Pathobiochemistry, University of Wuerzburg, D-97080 Wuerzburg, Germany
2Medical Hospital II, University of Wuerzburg, D-97080 Wuerzburg, Germany
3University Children’s Hospital, University of Wuerzburg, D-97080 Wuerzburg, Germany
4Laboratory for Microarray Applications, University of Wuerzburg, D-97080 Wuerzburg, Germany

Received 18 August 2010; Accepted 3 January 2011

Academic Editor: Donna-Marie McCafferty

Copyright © 2011 Claudia Beyrich 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.


Early onset sepsis due to group B streptococcus leads to neonatal morbidity, increased mortality, and long-term neurological deficencies. Interaction between septicemic GBS and confluent monolayers of human coronary artery endothelial cells (HCAECs) was analyzed by genome wide expression profiling. In total, 124 genes were differentially expressed (89 upregulated, 35 downregulated) based on a more than 3-fold difference to control HCAEC. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, infection, and inflammation. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real-time RT-PCR assay (granulocyte chemotactic protein 2), ELISA (urokinase, cyclooxygenase 2, granulocyte chemotactic protein 1), and western blotting (Heme oxygenase1, BCL2 interacting protein) at various time points between 4 and 24 hours. These results indicate that GBS infection might influence signalling pathways leading to impaired function of the innate immune system and hemorrhagic and inflammatory complications during GBS sepsis.