RESUMO
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. 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. 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. Glycans terminating in beta-galactose, terminal Galbeta1,3GalNAc and subsets of GalNAc also appeared in alveolar macrophages of fibrotic lung disorders. L-fucosylated and terminal alpha-linked galactosyl glycans were also detected in diseases states. Subsets of N-glycans were either changed minimally or not at all