Sulfated oligosaccharides isolated from the respiratory mucins of a secretor patient suffering from chronic bronchitis

被引:22
作者
Degroote, S
Maes, E
Humbert, P
Delmotte, P
Lamblin, G
Roussel, P
机构
[1] INSERM, U377, Dept Biochim, Fac Med, F-59045 Lille, France
[2] Univ Lille, F-59045 Lille, France
[3] Univ Sci & Tech Lille Flandres Artois, F-59655 Villeneuve Dascq, France
[4] CNRS, UMR 8576, Unite Glycobiol Structurale & Fonctionnelles, F-59655 Villeneuve Dascq, France
关键词
respiratory mucins; sulfated oligosaccharides; chronic bronchitis; cystic fibrosis;
D O I
10.1016/S0300-9084(03)00022-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The most acidic carbohydrate chains released by alkaline borohydride treatment of the bulk of airway mucins secreted by a patient (blood group O, secretor) suffering from a mildly infected chronic bronchitis have been fractionated using high-performance anion-exchange chromatography (HPAEC) according to a protocol already described [Lo-Guidice et al., J. Biol. Chem. 269 (1994) 18794] and were analyzed using H-1-NMR spectroscopy and matrix-assisted laser-adsorption-time-of-flight (MALDI-TOF) spectrometry. Many fractions corresponded to mixtures of oligosaccharides. This confirmed the wide diversity of the post-translational processes involved in the biosynthesis of airway mucins, which had already been observed in bronchial diseases, such as chronic bronchitis and cystic fibrosis (CF). Seven fractions were directly purified by HPAEC, allowing their structural determination. Six of them corresponded to 3-O-sulfated oligosaccharide chains terminated by a sulfated N-acetyllactosamine, a sulfated Lewis X or a sulfated Lewis A determinant, and the last one corresponded to a 6-O-sulfated chain terminated by a sulfated H-2 determinant. Three oligosaccharides had core type 2 and the other four had core type 4: IIIc2-9: Gal(beta1-3)[HSO3-3-Gal(beta1-4)GlcNAc(beta1-6)]GalNAc-ol IIIc2-10: Gal(beta1-3)[Fuc(alpha1-2)Gal(beta1-4)[HSO3-6-]GlcNAc(beta1-6)]GalNAc-ol IIIc2-4: Fuc(alpha1-2)Gal(beta1-3)[HSO3-3-Gal(beta1-4)[Fuc(alpha1-3)]GlcNAc(beta1-6)]GalNAc-ol IIIc2-8: Fuc(alpha1-2)Gal(beta1-3)GlcNAc(beta1-3)[HSO3-3-Gal(beta1-4)GlcNAc(beta1-6)]GalNAc-ol IIIc2-7: Fuc(alpha1-2)Gal(beta1-3)GlcNAc(beta1-3)[Gal(beta1-4)[HSO3-6-]GlcNAc(beta1-6)]GalNAc-ol IIIc2-3: Fuc(alpha1-2)Gal(beta1-3)GlcNAc(beta1-3)[HSO3-3-Gal(beta1-4)[Fuc(alpha1-3)]GlcNAc(beta1-6)]GalNAc-ol IIIc1-4: Fuc(alpha1-2)Gal(beta1-3)GlcNAc(beta1-3)[HSO3-3-Gal(beta1-3)[Fuc(alpha1-4)]GlcNAc(beta1-3)Gal(beta1-4)GlcNAc(beta1-6)]GalNAc-ol Like previous data concerning the airway mucins from another patient (blood group O and non-secretor) suffering from chronic bronchitis [Lo-Guidice et al., Glycoconj. J. 14 (1997) 1131, no disialylated oligosaccharide and no sialylated and sulfated oligosaccharide bearing sialyl Lewis X epitope could be isolated. This is in contrast with the data obtained with the airway mucins secreted by the patient severely infected by Pseudomonas aeruginosa and suffering from CF, suggesting that important differences occur in the biosynthesis of airway mucins secreted by patients suffering from different bronchial diseases with or without severe infection. (C) 2003 Editions scientifiques et medicales Elsevier SAS and Societe francaise de biochimie et biologie moleculaire. All rights reserved.
引用
收藏
页码:369 / 379
页数:11
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