Eosinophils, neutrophils, and venular gaps in the airway mucosa at epithelial removal-restitution

Jonas Erjefält, Frank Sundler, C G Persson

Research output: Contribution to journalArticlepeer-review


Shedding of epithelium, increased venular permeability, and traffic of activated eosinophils and neutrophils may characterize asthmatic airways. This in vivo study involving briefly anesthetized guinea pigs examines 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 membrane. After 10 min, 2, 8, and 48 h, the tracheal tissue was examined by scanning and transmission electron microscopy. Silver staining revealed endothelial cell borders. Histochemistry identified neutrophils and eosinophils. Confirming previous observations, epithelial restitution started promptly and occurred speedily under a plasma exudation-derived, leukocyte-rich gel. Ten minutes after de-epithelialization, venular gaps (silver dots) were recognized as plasma exudation sites and, separately, silver rings at endothelial cell borders indicated attachment and extravasation of leukocytes. Tissue neutrophils were increased from 10 min to 48 h. Normally occurring eosinophils decreased in numbers during re-epithelialization, partly due to migration into the airway lumen and local cell death. Clusters of extracellular eosinophil granules were increased from 10 min to 8 h. Gentle removal of airway epithelium 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 leukocyte changes that occur in inflammatory airway diseases.
Original languageEnglish
Pages (from-to)1666-1674
JournalAmerican Journal of Respiratory and Critical Care Medicine
Issue number5
Publication statusPublished - 1996

Bibliographical note

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Neuroendocrine Cell Biology (013212008), Airway Inflammation and Immunology (013212038)

Subject classification (UKÄ)

  • Respiratory Medicine and Allergy


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