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, Con A, 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 β- galactose, terminal Gal β1, 3 GalNAc and subsets of GalNAc also appeared in alveolar macrophages of fibrotic lung disorders. L- fucosylated and terminal α-linked galactosyl glycans were also detected in diseases states. Subsets of N- glycans were either changed minimally or not at all.