S. Varsano et al., NORMAL SERUM INCREASES ADHESION OF NEUTROPHILS TO TRACHEAL EPITHELIAL-CELLS BY A CD11B CD18-DEPENDENT MECHANISM/, American journal of respiratory cell and molecular biology, 10(3), 1994, pp. 298-305
Airway inflammation is characterized by intraluminal influx of inflamm
atory cells, exudation of plasma, and increased procoagulant activity.
We speculated that inflammatory cells might adhere to the airway surf
ace epithelium in order to better localize and regulate airway inflamm
atory responses. Therefore, in this study, we asked whether neutrophil
s adhere to airway epithelial cells, whether serum or plasma factors i
ncrease adhesion, and, if so, what the characteristics of the involved
adhesion molecules are. To answer these questions, we incubated human
Cr-51-labeled neutrophils from peripheral blood with dog tracheal epi
thelial cells in culture in the presence or absence of normal human se
rum 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 increa
sed 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 dival
ent cations. mAb 60.3 (anti-CD18) and mAb anti-Mo1 (anti-CD11b, anti-C
R3) inhibited serum-induced adhesion by > 50% each. We conclude that n
ormal serum and plasma contain a potent adhesion factor that induces a
dhesion of neutrophils to tracheal epithelium in culture. This factor
is most likely serum complement fragment iC3b. We speculate that in ai
rway inflammation, exudation of plasma and local activation of complem
ent system induces adhesion of neutrophils and, probably, of other pha
gocytic cells to airway epithelium at the site of insult. This may con
tribute to first-line airway mucosal defense.