Interleukin 1-β induces neutrophil adhesion to human pulmonary artery endothelial cells

Adhesion of polymorphonuclear leucocytes (PMNs) to pulmonary endothelium is an initial step in the inflammatory process characteristic of the Adult Respiratory Distress Syndrome (ARDS). Inhibition of the adhesion process has potential clinical applications in relation to inflammatory pulmonary disease. To date most studies examining PMN adhesion to endothelial cells have used human umbilical vein endothelial cells (HUVECs). Previous work (Davern S et al, Am J Resp Crit Care Med 1996, 153 (4):A617) has shown that LPS stimulated PMN do not adhere to human pulmonary artery endothelial cells, as they do to HUVECs. The aim of this study was to determine whether PMNs adhere to IL-1β stimulated HPAECs, as has been observed with HUVECs. Confluent HPAECs were pre-incubated with IL-1β, the cytokine washed off, PMNs added and adhesion calculated by measuring myeloperoxidase (MPO) content in adhered and nonadhered samples and expressing this as a % of total MPO. Significant adhesion (**p<0.01) of PMNs to HPAECs occurred even at the lowest concentration of IL-1β used (Table). Table Control IL-1β 2.5 U/ml 5 IL-1β U/ml 10 IL-1β U/ml IL-1β 20 U/ml Mean 28.15 52.84** 54.38* 58.5** 59.85** SEM 8.96 3.97 3.63 3.85 7.34 (Student Newman Keuls multiple comparisons test, n=5) These results suggest that upregulation of adhesion molecules on endothelial cells rather then on PMN may be of more significance in PMN adhesion to endothelial cells of pulmonary origin than to those of umbilical vein origin.