Am. J. Respir. Cell Mol. Biol., Vol 10, No. 3, 03 1994, 298-305.
Normal serum increases adhesion of neutrophils to tracheal epithelial cells by a CD11b/CD18-dependent mechanism
S Varsano, N Joseph-Lerner, T Reshef and I Frolkis
Department of Pulmonary Medicine, Sapir Medical Center, Meir General Hospital, Kfar Sava, Israel.
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)
