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Autocrine Loop of Endothelial Activation as an Intermediate Between Acute and Chronic Inflammation: an Experimental Model Involving Thrombin
*
Institut National de la Santé et de la Recherche Médicale Unité 387, Hôpital Sainte-Marguerite, and
Immunotech, a Beckman Coulter Company, Marseille, France
Thrombin is a procoagulant and proinflammatory molecule in vivo. In
vitro, thrombin has been shown to induce endothelial activation,
notably IL-8 secretion and adhesion molecule expression. In this study,
we showed that thrombin may induce a new cascade leading from acute to
chronic inflammation. Thrombin was able to induce the production of
both IL-6 and monocyte chemotactic protein-1 (MCP-1) by HUVEC
independently of IL-1
and TNF-. Addition of physiological
concentrations of exogenous soluble IL-6R (sIL-6R) to
thrombin-activated HUVEC was sufficient to increase the amounts of
MCP-1 produced, but not those of IL-8. These effects could be blocked
by anti-IL-6 or anti-sIL-6R blocking mAb, demonstrating the
existence of an autocrine loop of MCP-1 secretion, involving the
IL-6/IL-6R/gp130 complex on HUVEC. In addition, we identified
IL-8-activated neutrophils as a potential source of sIL-6R because
IL-8 induced IL-6R shedding from the neutrophil membranes and
increased in parallel sIL-6R concentrations in neutrophil
supernatants. Furthermore, addition of neutrophils to
thrombin-activated HUVEC significantly increased MCP-1 secretion, which
could be decreased by blocking IL-6. Thus, thrombin-activated
endothelium may induce a cascade of events characterized by IL-8
secretion, neutrophil local infiltration, and the release of IL-6R
from neutrophil membranes. sIL-6R may then complex with IL-6 and
increase the amount of MCP-1 produced by thrombin-activated
endothelium, favoring monocyte infiltration, and the transformation of
acute into chronic inflammation.
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