Article Text

Download PDFPDF

Cellular mechanisms in chronic lung disease
Free

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

S128 ALVEOLAR SEPTAE IN SEVERE END-STAGE EMPHYSEMA SHOW MORPHOLOGICAL EVIDENCE OF DYSREGULATED MESENCHYMAL CELL PROLIFERATION AND LOSS OF MICROVASCULARITY

1LS Mackay, 2K Pinnion, 2S Bolton, 1C Ward, 1J Lordan, 1AJ Fisher, 2M Foster, 1PA Corris. 1Applied Immunobiology and Transplantation Research Group, Freeman Hospital, Newcastle University, Newcastle upon Tyne, UK, 2Astrazeneca R&D, Charnwood, Loughborough, UK

Emphysema is defined as permanent enlargement of alveolar air spaces with loss of alveolar wall connectivity. This definition does not reflect the true complexity of histological phenotypes seen. In particular, septal thickening and matrix deposition have been recognised in alveolar septae. Changes in microvascular density also occur in alveolar septae and we therefore hypothesised that alteration in the phenotype of septal remodelling may be related to the loss of alveolar microvascularity.

Methods: Lung tissue resections were obtained from patients undergoing lung transplantation for emphysema (n  =  9) and compared with archival “normal” tissue obtained from lung cancer resections. All material was examined using haematoxylin and eosin stained sections to establish variations in lesion phenotypes. Mesenchymal cell distribution, matrix deposition and microvascularity were assessed by α-SMA, collagen I and CD31 immunohistochemistry, respectively. All emphysema lung material presented with wide heterogeneity in lesion phenotypes and so all of the section was examined.

Results: All emphysema sections presented with classic (distended, thin, disconnected) alveolar septae with focal areas of mesenchymal cell and matrix deposition. Thickened septae were also a very common feature in the emphysema group and more marked than in control samples. Two phenotypes were seen: acellular thickening, occupying the whole of the septal unit and a “reticular” pattern of mesenchymal cells and matrix occupying the external facets of the septal wall. Within these thickened zones there was loss of the normal anatomy of the microvasculature, with CD31 immunoreactivity seen as granular deposits within the expanded collagen zones or focal regions abutting the septal margins.

Conclusions: We …

View Full Text