Regulation of endothelial and mesothelial cell function by interleukin-13: selective induction of vascular cell adhesion molecule-1 and amplification of interleukin-6 production

• Published in: Blood Vol. 84; no. 6; pp. 1913 - 1921
• Main Authors: Sironi, M, Sciacca, F L, Matteucci, C, Conni, M, Vecchi, A, Bernasconi, S, Minty, A, Caput, D, Ferrara, P, Colotta, F
• Format: Journal Article
• Language: English
• Published: United States 15.09.1994
• Subjects: Base Sequence; Blotting, Northern; Cell Adhesion Molecules - biosynthesis; Cell Adhesion Molecules - genetics; E-Selectin; Endothelium, Vascular - physiology; Humans; Intercellular Adhesion Molecule-1; Interleukin-1 - pharmacology; Interleukin-13; Interleukin-6 - biosynthesis; Interleukin-6 - genetics; Interleukins - pharmacology; Mesoderm - physiology; Molecular Sequence Data; Monocytes - metabolism; Polymerase Chain Reaction; Recombinant Proteins - pharmacology; RNA, Messenger - biosynthesis; RNA-Directed DNA Polymerase; Vascular Cell Adhesion Molecule-1
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood.V84.6.1913.1913

The present study was designed to explore the interaction of interleukin-13 (IL-13) with vascular endothelial cells (EC). In vitro exposure to IL-13 of human umbilical vein EC induced surface expression of vascular cell adhesion molecule-1 (VCAM-1). At optimal concentrations (10 to 50 ng/mL) and exposure times (24 hours), IL-13 was a twofold to threefold less effective inducer of VCAM-1 than IL-1, which was used as reference EC activator. When IL-13 was combined with IL-1, an almost additive induction of VCAM-1 was observed. Induction of VCAM-1 by IL-13 was selective in that E-selectin and intercellular adhesion molecule-1 (ICAM-1) were unaffected. IL-13 caused a modest reduction of IL-1 induction of E-selectin and ICAM-1. Surface expression of VCAM-1 on IL-13-treated cells was associated with mRNA induction (as assessed by Northern analysis and reverse transcriptase-polymerase chain reaction), with predominance of transcripts encoding the 7 Ig domain form of this molecule. In agreement with previous reports, IL-13 inhibited cytokine production in human monocytes. In contrast, IL-13 was a weak inducer and an amplifier (in concert with IL-1) of IL-6 expression in EC. Mesothelial cells, which share properties with EC and regulate the traffic and function of leukocytes in serosal cavities, were stimulated to express VCAM-1 and IL-6 by IL-13. Thus, IL-13 elicits a spectrum of responses in vascular endothelium remarkably similar to that of IL-4 and IL-10. Interaction of these cytokines with vascular endothelium may play an important role in the induction and expression of Th2-dependent responses.