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  • Title: Modulation of the glycoconjugate expression in the tracheo-bronchial epithelium during sustained hypovitaminosis A.
    Author: Zschabitz A, Weiser H, Stofft E, Gabius HJ, Biesalski HK.
    Journal: Histol Histopathol; 1996 Apr; 11(2):395-405. PubMed ID: 8861763.
    Abstract:
    The aim of this study was to determine the influence of sustained marginal vitamin A deficiency on the morphology of glycoconjugate expression in the tracheobronchial epithelium of guinea pigs. The distribution of oligosaccharide chains was investigated by applying a panel of 24 lectins. Glycosaminoglycans were detected by histochemical techniques. Number as well as morphology of ciliated cells showed no significant alterations in hypovitaminosis A. In contrast, the quantity of goblet cells was constantly decreased. A considerable reduction of secretory granules was also observed in these cells. Cytomembranes of ciliated cells (especially in the area of ciliar extensions) showed constant alterations in the patterns of lectin binding in vitamin A-depleted guinea pigs. Our results demonstrate a significant augmentation of accessibility of fucosyl molecules in proximal domains of glycoconjugates of ciliary membranes, whereas the presence of mannose structures seemed unchanged. In distal bronchioli, terminal N-acetylgalactosamine molecules were expressed. During marginal vitamin A deficiency, ciliary cells were specially labelled by GSA I(B), indicating presentation of terminal galactose molecules in alpha-position. Additionally, the cytoplasm of epithelial cells demonstrated enhanced concentrations of polyantennary oligosaccharide core structures. Staining of epithelial cells by VVA was restricted to control specimens. Abundance of N-acetylglucosamine residues on the non-reducing terminus of oligosaccharides was significantly enhanced in the connective tissue of depleted animals as demonstrated by the binding patterns of GSA II. We suggest that altered oligosaccharide patterns may contribute to enhanced predisposition to tracheobronchial infection in marginal vitamin A deficiency.
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