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

In English

Författare

Summary, in English

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.

Publiceringsår

1996

Språk

Engelska

Sidor

1666-1674

Publikation/Tidskrift/Serie

American Journal of Respiratory and Critical Care Medicine

Volym

153

Issue

5

Dokumenttyp

Artikel i tidskrift

Förlag

American Thoracic Society

Ämne

  • Respiratory Medicine and Allergy

Status

Published

Forskningsgrupp

  • Airway Inflammation and Immunology

ISBN/ISSN/Övrigt

  • ISSN: 1535-4970