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

Originalveröffentlichung:

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

pdf-Format:

Dokument 1.pdf (722 KB)

SWD-Schlagwörter:		Medizin
Institut:		Institut für Klinische Biochemie und Pathobiochemie
DDC-Sachgruppe:		Medizin
Dokumentart:		Aufsatz / Artikel
Sprache:		Englisch
Erstellungsjahr:		2011
Publikationsdatum:		20.11.2012
Kurzfassung auf Englisch:		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.
Lizenz:		Creative Commons - Namensnennung

Eingang zum Volltext in OPUS