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细胞表面碳水化合物在体外调节中性粒细胞对II型肺泡细胞的黏附。

Cell surface carbohydrates modulate neutrophil adherence to alveolar type II cells in vitro.

作者信息

Crestani B, Rolland C, Petiet A, Colas-Linhart N, Aubier M

机构信息

Institut National de la Santé et de la Recherche Médicale U. 226, Paris, France.

出版信息

Am J Physiol. 1993 Apr;264(4 Pt 1):L391-400. doi: 10.1152/ajplung.1993.264.4.L391.

DOI:10.1152/ajplung.1993.264.4.L391
PMID:8476068
Abstract

We characterized the influence of phosphorylated sugars and cell surface sialic acids on the adherence of human polymorphonuclear leukocyte (PMN) to rat alveolar type II cell (ATII cells) and human-derived A549 cell monolayers in vitro. Percent adherence of radiolabeled polymorphonuclear leukocytes was assessed after incubating cells with the carbohydrates, enzymes, or lectins to be tested. Lactose-1-phosphate (Lact1P) and maltose-1-phosphate (Malt1P) (10 mM) inhibited adherence of PMN to ATII cells and A549 cells. Maximal inhibition followed treatment of both PMN and rat ATII cells and amounted to 85 +/- 7% with Lact1P and 92 +/- 3% with Malt1P. Inhibition was concentration dependent. Incubation of PMN with mannose-6-phosphate reduced adherence to rat ATII cells and A549 cells by 36 +/- 11 and 39 +/- 8%, respectively. Maximal concentrations of sugars did not alter cellular viability. Neuraminidase-induced desialilation of ATII cells increased adherence of PMN by 36 +/- 7% to rat ATII cells and by 86 +/- 18% to A549 cells. Masking of terminal sialic acids on rat ATH cells with Limulus polyphemus agglutinin (100 micrograms/ml) increased adherence by 50 +/- 2%. These results indicate that cell surface carbohydrates are involved in the regulation of the adhesive interaction between PMN and ATII cells in vitro.

摘要

我们在体外研究了磷酸化糖和细胞表面唾液酸对人多形核白细胞(PMN)与大鼠II型肺泡细胞(ATII细胞)及人源A549细胞单层黏附的影响。在用待测的碳水化合物、酶或凝集素孵育细胞后,评估放射性标记的多形核白细胞的黏附百分比。1 - 磷酸乳糖(Lact1P)和1 - 磷酸麦芽糖(Malt1P)(10 mM)可抑制PMN与ATII细胞及A549细胞的黏附。对PMN和大鼠ATII细胞进行处理后,抑制作用达到最大值,Lact1P的抑制率为85±7%,Malt1P为92±3%。抑制作用呈浓度依赖性。用6 - 磷酸甘露糖孵育PMN后,其与大鼠ATII细胞及A549细胞的黏附分别减少36±11%和39±8%。糖的最大浓度不会改变细胞活力。神经氨酸酶诱导的ATII细胞去唾液酸化使PMN与大鼠ATII细胞的黏附增加36±7%,与A549细胞的黏附增加86±18%。用鲎试剂凝集素(100微克/毫升)封闭大鼠ATII细胞上的末端唾液酸,可使黏附增加50±2%。这些结果表明,细胞表面碳水化合物参与了体外PMN与ATII细胞间黏附相互作用的调节。

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