Thrombin enhancement of interleukin-1 expression in mononuclear cells: involvement of proteinase-activated receptor-1

Cytokine. 2002 Dec 7;20(5):191-9. doi: 10.1006/cyto.2002.2001.

Abstract

In addition to its central role in blood coagulation and hemostasis, human alpha-thrombin is considered a pro-inflammatory molecule. We have previously demonstrated that differentiated monocytes express the proteolytically activated receptor for thrombin (PAR-1) and that thrombin enhances the release of interleukin (IL)-6 in human monocytes. In the present study we show that thrombin upregulates the production of both IL-1alpha and IL-1beta in phytohemagglutin (PHA)-activated human peripheral blood mononuclear cells (PBMC). Treating PHA-activated PBMC with the PAR-1 activation peptide, SFLLRN, mimics the effects of thrombin on IL-1alpha and IL-1beta production. Thus, it appears that these pro-inflammatory effects induced by thrombin may be mediated through activation of PAR-1. ELISA and RNase protection assays indicate that thrombin and SFLLRN peptide upregulates IL-1 expression at both protein and mRNA levels. Thrombin directly affects monocyte IL-1 expression, since treatment of differentiated U937 cells with thrombin and SFLLRN enhances IL-1 production. These results may help explain how thrombin can enhance IL-1 expression in normal tissue to initiate tissue repair and why thrombin and thrombin-like enzymes may contribute to inflammatory responses observed in several pathophysiological conditions.

MeSH terms

  • Humans
  • Interleukin-1 / biosynthesis
  • Interleukin-1 / genetics*
  • Leukocytes, Mononuclear / metabolism*
  • RNA, Messenger / metabolism
  • Receptor, PAR-1
  • Receptors, Thrombin / metabolism*
  • Thrombin / metabolism*
  • Up-Regulation

Substances

  • Interleukin-1
  • RNA, Messenger
  • Receptor, PAR-1
  • Receptors, Thrombin
  • Thrombin