Salmonella infection and proinflammatory responses of human vascular endothelial cells

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Salmonella infection of human vascular endothelial cells and its role of as a stimulus for endothelial cell activation have been studies. Invasion of cultured HUVEC monolayers was dependent of the Salmonella invasion locus, Salmonella pathogenicity island 1 (SPI-1). The wild-type RF-1 strain of Salmonella enterica serovar Choleraesuis was efficiently internalized by HUVEC whereas the invasiveness of an isogenic invA mutant decreased to 30% of the wild-type strain. When analyzed by a reverse transcriptase PCR method, infection of HUVEC with invasive, but not noninvasive, bacteria resulted in increased expression of mRNA for the cytokine IL-8. In addition, Salmonella stimulated surface expression of E-selectin (CD62E), ICAM-1 (CD54) and VCAM-1 (CD106). These results may indicate that invasion of endothelial cells by Salmonella is a mechnisms for triggering local vascular inflammation.