Hocl effects on the tight junctions of rabbit tracheal
epithelium.
Guo, Yi, Marcy Krumwiede, James G. White, O. Douglas Wangensteen.
Departments of Physiology, Pediatrics and Laboratory Medicine and
Pathology, University of Minnesota, Minneapolis, MN 55455
APStracts 2:0156L, 1995.
We previously found that HOCl, produced from neutrophil products in
infected airways, decreases electrical resistance (R) of rabbit
tracheal epithelium. Interestingly, 6 mM HOCl, a reasonable
concentration in diseased airways, decreased R without apparent cell
damage. This study sought to determine whether this non-cytotoxic
dose of HOCl causes morphologic changes that correlate with the
decrease in R. Excised rabbit tracheas were treated with 6 mM HOCl
for 15 min, before and after which epithelial R was determined.
Epithelial tissue was then fixed and prepared for: transmission
electron microscopy, immuno-fluorescent labelling of f-actin or the
tight junction protein ZO-1, or freeze-fracture to examine tight
junction strands. HOCl treatment caused a 50% decrease in R. Electron
micrographs showed no cell, cell membrane or tight junction changes.
By laser confocal microscopy, 6 mM HOCl did not affect the
distribution of either f-actin or ZO-1. However, morphometric
analysis of freeze-fracture replicas showed tight junction strand
number was significantly decreased from 7.06+/-0.09 to 4.79+/-0.11,
and junctional width was significantly decreased from 0.306+/- 0.007
Nm to 0.214+/-0.006 Nm. These latter changes may have contributed to
the observed decrease in epithelial electrical resistance.
Received 19 June 1995; accepted in final form 24 August 1995.
APS Manuscript Number L192-5.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.