Volume 14, Issue 1 (Spring 2007 2006)                   JSSU 2006, 14(1): 41-46 | Back to browse issues page

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Abstract:   (20669 Views)
Introduction: The respiratory system is both a route of entry and exit for toxins and injurious agents, as well as being a target for chemical substances and pathogens. Therefore, an understanding of the structure and function of the migratory cell populations of pulmonary tissues including alveolar macrophages is central in a number of important disease processes. This study aimed to identify and specify the glycotypes of alveolar macrophages in fibrotic lung disorders. Methods: Sections of paraffin-embedded tissue from 40 cases in both normal human lung and fibrotic lung disorders were studied by immunohistology and by lectin histochemistry with a panel of 27 biotinylated lectins. Results: The findings of this study showed that ten lectins (AHA, PTL-II, AAA, , LTA, UEA-I, BSA-1B4, VVA, SBA, DBA, PTL-I) did not bind to the alveolar macrophages in any of the cases, whereas 17 lectins (GNA, NPA, HHA, l-PHA, e-PHA, LCA, PSA, ConA, LEA, PAA, s-WGA, ECA, MPA,HPA, WFA, SNA, MAA( bound from moderately to strongly. In contrast, in fibrotic lung disorders some glycans were somewhat more marked or changed. Conclusion: Glycans terminating in -galactose, terminal Gal1,3GalNAc and subsets of GalNAc also appeared in alveolar macrophages of fibrotic lung disorders. L-fucosylated and terminal -linked galactosyl glycans were also detected in diseases states. Subsets of N-glycans were either changed minimally or not at all.
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Type of Study: Original article | Subject: General
Received: 2010/01/25 | Published: 2006/04/15