Production of a retroviral P15E-related chemotaxis inhibitor by IL-1-treated endothelial cells. A possible negative feedback in the regulation of the vascular response to monokines

J. M. Wang, Z. G. Chen, G. J. Cianciolo, R. Snyderman, F. Breviario, E. Dejana, A. Mantovani

Research output: Contribution to journalArticle

Abstract

The effects of IL-1 on vascular endothelium result in a complex set of alterations which are potentially disruptive of vessel wall and underlying tissue integrity. The present study was aimed at investigating possible regulation of such potentially destructive responses elicited by IL-1 on endothelial cells. Culture supernatants of IL-1-treated human umbilical vein endothelial cells (HEC) were depleted of retroviral p15E-related Ag with immobilized anti-p15E mAb. The monocyte chemotactic and polarizing activity of supernatants of IL-1-treated HEC (presumably related to colony-stimulating factors being released by HEC) was markedly augmented by absorption on immobilized anti-p15E antibodies. Irrelevant IgG had no effect and anti-p15E antibodies did not affect the chemotactic activity of supernatants from unstimulated HEC. The material eluted from Sepharose-bound anti-p15E antibodies was devoid of chemotactic and polarizing activity and suppressed the polarization and migration of monocytes in response to chemoattractants. The α and β molecular species of IL-1 were equally effective in inducing the production of p15E-related inhibitor. The production of a p15E-related inhibitor of chemotaxis induced by IL-1 in HEC may represent a negative signal in the regulation of the potentially destructive responses to pro-inflammatory cytokines.

Original languageEnglish
Pages (from-to)2012-2017
Number of pages6
JournalJournal of Immunology
Volume142
Issue number6
Publication statusPublished - 1989

ASJC Scopus subject areas

  • Immunology

Fingerprint Dive into the research topics of 'Production of a retroviral P15E-related chemotaxis inhibitor by IL-1-treated endothelial cells. A possible negative feedback in the regulation of the vascular response to monokines'. Together they form a unique fingerprint.

  • Cite this