study of changes in cellular surface glycoproteins of alveolar macrophages in fibrotic lung disorders

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.