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Blood, 1 January 2002, Vol. 99, No. 1, pp. 185-192
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Cytolytically inactive terminal complement complex causes
transendothelial migration of polymorphonuclear leukocytes in vitro and
in vivo
Aldo Dobrina,
Mario Pausa,
Fabio Fischetti,
Roberta Bulla,
Elena Vecile,
Elisabetta Ferrero,
Alberto Mantovani, and
Francesco Tedesco
From the Dipartimento di Fisiologia e Patologia, the
Dipartimento di Medicina Clinica e Neurologia, Università di
Trieste, the IRCCS Burlo Garofolo, Trieste, Italy; the IRCCS H. San
Raffaele, the Istituto di Patologia Generale, and the Istituto di
Ricerche Farmacologiche Mario Negri, Milan, Italy.
Intravital microscopy was used to monitor leukocyte traffic across
rat mesenteric postcapillary venules induced by the inactive terminal
complement (C) complex (iTCC) topically applied to ileal mesentery.
Leukocytes started rolling within 15 minutes from the administration of
iTCC, and by 1 hour they adhered almost completely to the endothelium
emigrating from the vessels in the next 3 hours. C5a caused a similar,
though less marked, effect, whereas boiled iTCC was inactive, excluding
the contribution of contaminating lipopolysaccharide. The complex
stimulated the migration of polymorphonuclear neutrophils (PMNs) across
endothelial cells (ECs) in a transwell system after a 4-hour incubation
of ECs with iTCC added to the lower chamber of the transwell, whereas a
30-minute incubation was sufficient for C5a and interleukin (IL)-8 to
induce the passage of PMNs. C5a was not responsible for the effect of
iTCC because this complex had no chemotactic activity and contained too
small an amount of C5a to account for the transendothelial migration of
PMNs. Similarly, the effect of iTCC was not mediated by IL-8 released
by stimulated ECs because anti-IL-8 failed to inhibit the migration of
PMNs induced by the complex. Unlike tumor necrosis factor- , iTCC did
not cause the redistribution of platelet-endothelial cell adhesion
molecule-1 (PECAM-1), and PMN mobilization was partially blocked by
anti-PECAM-1 antibodies.
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