Article date: October 1993
By: Carolyn A. Herbert, David Edwards, John R. Boot, Clive Robinson, in Volume 110, Issue 2, pages 840-846
The apical to basolateral transmucosal flux of albumin has been measured in isolated sheets of bovine bronchial and tracheal mucosa. Under resting conditions the net unidirectional flux in the bronchial mucosa was not significantly different from that measured previously for the basolateral to apical vector. In contrast, the apical to basolateral flux in the tracheal mucosa was significantly lower than that measured in the opposite direction.
Addition of guinea‐pig peritoneal eosinophils to the apical side of the tissues had no significant effect on the transmucosal flux of albumin in either the bronchial or tracheal mucosa.
When eosinophils were stimulated with the ionophore A23187 or by opsonic adherence to tissues treated with a guinea‐pig anti‐bovine airway epithelium antibody, the bronchial mucosal sheets that had been exposed showed a significant increase in the transmucosal flux of albumin. However, tissues from the tracheal mucosa were resistant to the effects of stimulated eosinophils.
Histologically, sheets of mucosa from bovine main bronchi that had been exposed to stimulated eosinophils were characterized by epithelial injury consisting of loss of columnar epithelium from the underlying basal cell layer and biomatrix. Much less evidence of cellular injury was observed in tracheal tissues.
Bacterial collagenases applied to the apical side of the sheets were shown to increase the permeability of the bronchial mucosa to albumin and to produce histological changes that had similarities with the pattern of damage produced by stimulated eosinophils.
These observations demonstrate that the ability of eosinophils to injure the bronchial mucosa is independent of the side of the tissue on which they are present. Furthermore, key aspects of the injury process may be reproduced, at least in part, by metalloproteinases.
The apical to basolateral transmucosal flux of albumin has been measured in isolated sheets of bovine bronchial and tracheal mucosa. Under resting conditions the net unidirectional flux in the bronchial mucosa was not significantly different from that measured previously for the basolateral to apical vector. In contrast, the apical to basolateral flux in the tracheal mucosa was significantly lower than that measured in the opposite direction.
Addition of guinea‐pig peritoneal eosinophils to the apical side of the tissues had no significant effect on the transmucosal flux of albumin in either the bronchial or tracheal mucosa.
When eosinophils were stimulated with the ionophore A23187 or by opsonic adherence to tissues treated with a guinea‐pig anti‐bovine airway epithelium antibody, the bronchial mucosal sheets that had been exposed showed a significant increase in the transmucosal flux of albumin. However, tissues from the tracheal mucosa were resistant to the effects of stimulated eosinophils.
Histologically, sheets of mucosa from bovine main bronchi that had been exposed to stimulated eosinophils were characterized by epithelial injury consisting of loss of columnar epithelium from the underlying basal cell layer and biomatrix. Much less evidence of cellular injury was observed in tracheal tissues.
Bacterial collagenases applied to the apical side of the sheets were shown to increase the permeability of the bronchial mucosa to albumin and to produce histological changes that had similarities with the pattern of damage produced by stimulated eosinophils.
These observations demonstrate that the ability of eosinophils to injure the bronchial mucosa is independent of the side of the tissue on which they are present. Furthermore, key aspects of the injury process may be reproduced, at least in part, by metalloproteinases.
DOI: 10.1111/j.1476-5381.1993.tb13889.x
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