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

Beyrich, Claudia ; Löffler, Jürgen ; Kobsar, Anna ; Speer, Christian P. ; Kneitz, Susanne ; Eigenthaler, Martin

Source:

(2011) In: Mediators of inflammation (2011), Article ID 971502, 8 p. doi:10.1155/2011/971502

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Dokument 1.pdf (722 KB)

Keywords from authority file SWD (German):		Medizin
Institute:		Institute of Clinical Biochemistry and Pathobiochemistry
Dewey Decimal Classification:		Medical sciences Medicine
Document type:		Article
Language:		English
Year of creation:		2011
Date of publication:		20.11.2012
Abstract in English:		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 (granulocy te 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.
License:		Creative Commons - Attribution

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