C5a Stimulates Eosinophil Adhesion to Human Lung Microvascular Endothelial or Epithelial Cells: Priming with TNFα or IL-5

Abstract

Eosinophils are thought to play a key role in perpetuating inflammatory changes and airway epithelial damage seen in asthma. Binding of eosinophils to endothelial cell adhesion molecules facilitates the migration of these cells from blood vessels into the respiratory tract. Subsequent eosinophil adhesion to airway epithelium may contribute to epithelial damage. A knowledge of factors that may potentiate or “prime” eosinophil adhesion to endothelial or epithelial cells may have important implications for the development of new anti-asthma therapies. For example, it has been shown that transendothelial migration of eosinophils in vitro can be “primed” by cytokines such as interleukin-5 (IL-5), IL-3 or GM-CSF [1]. We have recently shown, in vivo, that tumor necrosis factor α (TNFα) causes priming of eosinophil accumulation in guinea pig skin [2]. In the present in vitro study we have investigated priming effects of TNFα or IL-3 on C5a-induced adhesion of human eosinophils to human lung microvascular endothelial cells (LMVEC) or to a lung epithelial cell line (A549), in culture.