Normal serum increases adhesion of neutrophils to tracheal epithelial cells by a CD11b/CD18-dependent mechanism.

Airway inflammation is characterized by intraluminal influx of inflammatory cells, exudation of plasma, and increased procoagulant activity. We speculated that inflammatory cells might adhere to the airway surface epithelium in order to better localize and regulate airway inflammatory responses. Therefore, in this study, we asked whether neutrophils adhere to airway epithelial cells, whether serum or plasma factors increase adhesion, and, if so, what the characteristics of the involved adhesion molecules are. To answer these questions, we incubated human 51Cr-labeled neutrophils from peripheral blood with dog tracheal epithelial cells in culture in the presence or absence of normal human serum or plasma. After 30 min, nonadhering neutrophils were centrifuged away and neutrophil adhesion was assessed by radioassay. We found that unstimulated adhesion of neutrophils to cultured epithelial cells was quite low (< 6%). However, incubation with 10% serum or plasma increased adhesion of neutrophils to epithelial cells dramatically (up to a mean of 71%). The serum-induced increase in adhesion was concentration dependent; even 1% serum was effective (19% adhesion). Serum adhesion factor acted selectively on epithelial surfaces, was heat sensitive, had a molecular weight > 12,000, and depended on the presence of divalent cations. mAb 60.3 (anti-CD18) and mAb anti-Mol (anti-CD11b, anti-CR3) inhibited serum-induced adhesion by > 50% each. We conclude that normal serum and plasma contain a potent adhesion factor that induces adhesion of neutrophils to tracheal epithelium in culture.(ABSTRACT TRUNCATED AT 250 WORDS)