title: Failure to detect type 1 interferon production in human umbilical cord vein endothelial cells after viral exposure.
abstract: Cytokine production by endothelial cells is known to occur after the reception of signals such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). In the present study, we demonstrate cytokine release and upregulation of adhesion molecule expression of human endothelial cells derived from umbilical cord veins in response to stimulants. The cells were exposed to the plant lectin phytohemagglutinin A (PHA), the viral inducers Newcastle disease virus (NDV) and Sendai virus, and the nucleic acid analog polyinosinic/polycytidylic acid (polyI:C). All stimulants induced expression of IL-1 beta and IL-6. The titers of these cytokines were comparable to those obtained in human leukocytes, whereas no TNF-alpha release was detectable. A further feature of activation was upregulation of intercellular adhesion molecule 1 (ICAM-1), which was analyzed after contact with these stimulants. These experiments revealed an increased expression of ICAM-1 in response to all stimulants tested. A major part of our studies was devoted to the ability of endothelial cells to produce interferons as an important function of a number of cell types in response to viral infections. To ensure stimulation of the cells, the inducers NDV, Sendai virus, and polyI:C were analyzed. Expression of interferon (IFN) was not detected, although viral inducers mediated the release of IL-1 beta and IL-6, suggesting that endothelial cells are quite responsive to these stimulants. In conclusion, these findings show that the ability of endothelial cells to secrete cytokines is not restricted to mediators of the immune system, such as IL-1.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Institute of Immunology and Transfusion Medicine, University of Lübeck School of Medicine, Germany.
authors.forename: P
authors.initials: P
authors.lastname: Neustock
authors.forename: A
authors.initials: A
authors.lastname: Kruse
authors.forename: G
authors.initials: G
authors.lastname: Bein
authors.forename: S
authors.initials: S
authors.lastname: Nissen
authors.forename: H
authors.initials: H
authors.lastname: Kirchner
mesh_terms: D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D007370:Interferon Type I / Q000096:biosynthesis*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000096:biosynthesis; D016899:Interferon-beta / Q000096:biosynthesis; D007375:Interleukin-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology; D016169:Lymphocyte Function-Associated Antigen-1 / Q000096:biosynthesis; D009522:Newcastle disease virus / Q000276:immunology*; D010222:Parainfluenza Virus 1, Human / Q000276:immunology*; D010835:Phytohemagglutinins / Q000494:pharmacology; D011070:Poly I-C / Q000494:pharmacology; D011994:Recombinant Proteins; D014471:Umbilical Veins / Q000187:drug effects / Q000276:immunology*
chemical_list: D007370:Interferon Type I; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D007375:Interleukin-1; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016169:Lymphocyte Function-Associated Antigen-1; D010835:Phytohemagglutinins; D011994:Recombinant Proteins; D018799:Intercellular Adhesion Molecule-1; D016899:Interferon-beta; D011070:Poly I-C