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Department of Surgery, Duke University, Durham, NC 27710
Activation of complement in the vicinity of endothelium is thought
to contribute to the tissue manifestations of inflammatory and immune
responses. Endothelial cells contribute to these processes in part by
the elaboration of chemokines that activate various leukocytes and
direct their migration into tissues. We investigated the mechanisms by
which activation of complement on endothelial cell surfaces might
influence the expression of chemokine genes in endothelial cells. In a
model for the immune reaction occurring in a xenograft, human serum, as
a source of xenoreactive anti-endothelial Abs and complement,
induced expression of the monocyte chemotactic protein-1 (MCP-1), IL-8,
and RANTES genes. The MCP-1 and IL-8 genes were expressed within 3
h as a first phase and at >12 h as a second phase. The RANTES gene was
expressed in porcine endothelial cells only 12 h after exposure to
human serum. The expression of these genes required activation of
complement and assembly of membrane attack complex, as it was inhibited
by soluble CR1 and did not occur in the absence of C8. The early phase
of MCP-1 and IL-8 gene expression did not require de novo protein
synthesis. The late phase of MCP-1, IL-8, and RANTES gene expression
predominantly required the production of IL-1
as an intermediate
step. The results indicate that the expression of chemokine genes in
endothelial cells occurs as a function of differential responses to
complement and may in part be conditioned by the availability of
IL-1.
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