Transforming growth factor-beta increases Escherichia coli K1 adherence, invasion, and transcytosis in human brain microvascular endothelial cells.
Escherichia coli K1 traversal of the human brain microvascular endothelial cells (HBMEC) that constitute the blood-brain barrier (BBB) is a complex process involving E. coli adherence to and invasion of HBMEC. In this study, we demonstrated that human transforming growth factor-beta-1 (TGF-beta1) increases E. coli K1 adherence, invasion, and transcytosis in HBMEC. In addition, TGF-beta1 increases RhoA activation and enhances actin condensation in HBMEC. We have previously shown that E. coli K1 invasion of HBMEC requires phosphatidylinositol-3 kinase (PI3K) and RhoA activation. TGF-beta1 increases E. coli K1 invasion in PI3K dominant-negative HBMEC, but not in RhoA dominant-negative HBMEC, indicating that TGF-beta1-mediated increase in E. coli K1 invasion is RhoA-dependent, but not PI3K-dependent. Our findings suggest that TGF-beta1 treatment of HBMEC increases E. coli K1 adherence, invasion, and transcytosis, which are probably dependent on RhoA.
Zhang
Wen Guang
WG
Pediatric Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Khan
Ahmed Naveed
AN
Kim
Kee Jun
KJ
Stins
Monique
M
Kim
Kwang Sik
KS
D001921:Brain / Q000098:blood supply / Q000382:microbiology*; D002448:Cell Adhesion / Q000187:drug effects*; D002465:Cell Movement / Q000187:drug effects*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000382:microbiology*; D004789:Enzyme Activation / Q000187:drug effects; D004926:Escherichia coli / Q000187:drug effects / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D016212:Transforming Growth Factor beta / Q000494:pharmacology*; D020742:rhoA GTP-Binding Protein / Q000187:drug effects / Q000378:metabolism
D016212:Transforming Growth Factor beta; D020742:rhoA GTP-Binding Protein