Js. Erjefalt et al., EOSINOPHILS, NEUTROPHILS, AND VENULAR GAPS IN THE AIRWAY MUCOSA AT EPITHELIAL REMOVAL-RESTITUTION, American journal of respiratory and critical care medicine, 153(5), 1996, pp. 1666-1674
Citations number
44
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
Shedding of epithelium, increased venular permeability, and traffic of
activated eosinophils and neutrophils may characterize asthmatic airw
ays. This in vivo study involving briefly anesthetized guinea pigs exa
mines whether epithelial denudation itself affects airway venules and
granulocytes. Using an oral probe, a de-epithelialized tracheal zone (
0.8 x 30 mm) was produced without bleeding or damage to the basement m
embrane. After 30 min, 2, 8, and 48 h, the tracheal tissue was examine
d by scanning and transmission electron microscopy. Silver staining re
vealed endothelial cell borders. Histochemistry identified neutrophils
and eosinophils. Confirming previous observations, epithelial restitu
tion started promptly and occurred speedily under a plasma exudation-d
erived, leukocyte-rich gel. Ten minutes after de-epithelialization, ve
nular gaps (silver dots) were recognized as plasma exudation sites and
, separately, silver rings at endothelial cell borders indicated attac
hment and extravasation of leukocytes. Tissue neutrophils were increas
ed from 30 min to 48 h. Normally occurring eosinophils decreased in nu
mbers during re-epithelialization, partly due to migration into the ai
rway lumen and local cell death. Clusters of extracellular eosinophil
granules were increased from 10 min to 8 h. Gentle removal of airway e
pithelium thus produced venular gaps, infiltration of neutrophils, and
migration, activation, and death of eosinophils. Epithelial shedding-
restitution processes may cause part of the microvascular and leukocyt
e changes that occur in inflammatory airway diseases.