title: Divergent responses of different endothelial cell types to infection with Candida albicans and Staphylococcus aureus.
abstract: Endothelial cells are important in the pathogenesis of bloodstream infections caused by Candida albicans and Staphylococcus aureus. Numerous investigations have used human umbilical vein endothelial cells (HUVECs) to study microbial-endothelial cell interactions in vitro. However, the use of HUVECs requires a constant supply of umbilical cords, and there are significant donor-to-donor variations in these endothelial cells. The use of an immortalized endothelial cell line would obviate such difficulties. One candidate in this regard is HMEC-1, an immortalized human dermal microvascular endothelial cell line. To determine if HMEC-1 cells are suitable for studying the interactions of C. albicans and S. aureus with endothelial cells in vitro, we compared the interactions of these organisms with HMEC-1 cells and HUVECs. We found that wild-type C. albicans had significantly reduced adherence to and invasion of HMEC-1 cells as compared to HUVECs. Although wild-type S. aureus adhered to and invaded HMEC-1 cells similarly to HUVECs, an agr mutant strain had significantly reduced invasion of HMEC-1 cells, but not HUVECs. Furthermore, HMEC-1 cells were less susceptible to damage induced by C. albicans, but more susceptible to damage caused by S. aureus. In addition, HMEC-1 cells secreted very little IL-8 in response to infection with either organism, whereas infection of HUVECs induced substantial IL-8 secretion. This weak IL-8 response was likely due to the anatomic site from which HMEC-1 cells were obtained because infection of primary human dermal microvascular endothelial cells with C. albicans and S. aureus also induced little increase in IL-8 production above basal levels. Thus, C. albicans and S. aureus interact with HMEC-1 cells in a substantially different manner than with HUVECs, and data obtained with one type of endothelial cell cannot necessarily be extrapolated to other types.
authors: Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States of America.
authors: Kati
authors: K
authors: Seidl
authors: Norma V
authors: NV
authors: Solis
authors: Arnold S
authors: AS
authors: Bayer
authors: Wessam Abdel
authors: WA
authors: Hady
authors: Steven
authors: S
authors: Ellison
authors: Meredith C
authors: MC
authors: Klashman
authors: Yan Q
authors: YQ
authors: Xiong
authors: Scott G
authors: SG
authors: Filler
mesh_terms: D002176:Candida albicans / Q000472:pathogenicity*; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism / Q000382:microbiology*; D054884:Host-Pathogen Interactions; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism / Q000382:microbiology*; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism; D013211:Staphylococcus aureus / Q000472:pathogenicity*
chemical_list: D016209:Interleukin-8