The relapsing fever spirochaete, Borrelia crocidurae, activates human endothelial cells and promotes the transendothelial migration of neutrophils

The blood-borne, erythrocyte-aggregating Borrelia crocidurae, the causative agent of African relapsing fever, have been shown to induce severe cellula r lesions in mice. In this paper, we present the first report of how the en dothelium is stimulated during an African relapsing fever B, crocidurae inf ection. B, crocidurae co-incubated with cultured human umbilical vein endot helial cells (HUVECs) activated endothelium in such way that E-selectin and intercellular adhesion molecule 1 (ICAM-1) became upregulated in a dose- a nd time-dependent fashion, as determined by a whole-cell enzyme-linked immu nosorbent assay (ELISA). The upregulation was reduced by treatment that kil led the bacteria, suggesting that viability is important for the stimulatio n of HUVECs by B. crocidurae, Furthermore, conditioned medium from HUVECs s timulated with B. crocidurae contained interleukin (IL)-8, which is a chemo tactic agent for neutrophils, Activation of HUVECs by B. crocidurae resulte d in migration of subsequently added neutrophils across the endothelial mon olayers, and this migration was inhibited by antibodies to IL-8, The activa tion of endothelium by B. crocidurae may constitute a key pathophysiologica l mechanism in B. crocidurae-induced vascular damage.