No abstract

؉ RO ؉ cells. The migratory population was also enriched for CD8 ؉ T lymphocytes when the endothelium was incubated with either control medium or B. burgdorferi, but not IL-1. B. burgdorferi thus activates endothelium in a manner that promotes the transmigration of T lymphocytes, and IL-10 inhibits this activation. These data further suggest that endothelium plays an active role in promoting the recruitment of specific subpopulations of T lymphocytes.

The blood‐borne, erythrocyte‐aggregating Borrelia crocidurae, the causative agent of African relapsing fever, have been shown to induce severe cellular lesions in mice. In this paper, we present the first report of how the endothelium is stimulated during an African relapsing fever B. crocidurae infection. B. crocidurae co‐incubated with cultured human umbilical vein endothelial cells (HUVECs) activated endothelium in such way that E‐selectin and intercellular adhesion molecule 1 (ICAM‐1) became upregulated in a dose‐ and time‐dependent fashion, as determined by a whole‐cell enzyme‐linked immunosorbent assay (ELISA). The upregulation was reduced by treatment that killed the bacteria, suggesting that viability is important for the stimulation of HUVECs by B. crocidurae. Furthermore, conditioned medium from HUVECs stimulated with B. crocidurae contained interleukin (IL)‐8, which is a chemotactic agent for neutrophils. Activation of HUVECs by B. crocidurae resulted in migration of subsequently added neutrophils across the endothelial monolayers, and this migration was inhibited by antibodies to IL‐8. The activation of endothelium by B. crocidurae may constitute a key pathophysiological mechanism in B. crocidurae‐induced vascular damage.