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Published ahead of print on January 13, 2006, doi:10.1164/rccm.200509-1434OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 6, March 2006, 632-638

A more recent version of this article appeared on March 15, 2006
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Submitted on September 13, 2005
Accepted on January 9, 2006

Alteration of Fibroblast Architecture and Loss of Basal Lamina Apertures in Human Emphysematous Lung

Faye E Sirianni1, Alireza Milaninezhad1, Fanny S.F. Chu1, and David C Walker1*

1 Department of Pathology and Laboratory Medicine, University of British Columbia, The James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, Vancouver, BC, Canada

* To whom correspondence should be addressed. E-mail: dwalker{at}mrl.ubc.ca.

RATIONALE: In normal human lung, single alveolar fibroblasts link capillary endothelium to type 2 pneumocytes through apertures in the endothelial and epithelial basal laminae. These fibroblasts are hypothesized to play a role in cellular communication between the endothelium and epithelium and are positioned to provide leukocytes a surface upon which they may migrate through the interstitium. OBJECTIVES: To determine whether fibroblasts link the endothelium to the epithelium in emphysematous lung and to compare basal lamina aperture frequency with previously published results. METHODS: We performed TEM serial section 3D reconstructions of emphysematous regions of human alveolar wall and a quantitative analysis of basal lamina apertures beneath 403 Type 2 pneumocytes. MEASUREMENTS AND MAIN RESULTS: Our 3D reconstruction demonstrated that the fibroblasts subtending Type 2 pneumocytes in emphysematous lung no longer link these epithelial cells to the capillary endothelium through basal lamina apertures. In fact, basal lamina apertures may be completely absent below some Type 2 pneumocytes. Our morphometric analysis showed that their frequency and area beneath Type 2 pneumocytes is significantly reduced in emphysematous regions when compared to non-emphysematous regions of matched control lung. CONCLUSIONS: We conclude that the endothelial/fibroblast/epithelial linkage is disrupted in emphysematous human lungs and postulate this disruption may disturb leukocyte migration and account for their accumulation in the alveolar interstitium of emphysematous lung tissue.
Key words: emphysema, fibroblasts, leukocyte migration, basal lamina apertures, transmission electron microscopy




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