Mason C M, Azizi S Q, Dal Nogare A R
Department of Pulmonary and Critical Care Medicine, University of Texas Southwestern Medical Center, Dallas.
J Lab Clin Med. 1992 Nov;120(5):740-5.
One mechanism by which severe illness or stress might facilitate adherence and colonization of GNB to respiratory epithelium is by altering epithelial cell surface carbohydrates. To investigate this possibility we used radiolabeled lectins to quantitate carbohydrate levels on intact buccal and tracheal epithelium. A rat model of GNB colonization, in which renal infarction was performed to produce colonization, was used. Buccal and tracheal epithelial surface carbohydrate levels from normal rats and rats 48 hours after renal infarction were compared. Buccal and tracheal epithelium from the renal infarction animals had decreased amounts of sialic acid and fucose, and decreased levels of these sugars occurred at the same time that heavy oropharyngeal GNB colonization developed. Tracheas obtained from the infarcted animals bound three times more Type 1 piliated GNB than normal tracheas. Sialic acid and fucose levels are decreased early after stress, and we speculate that altered epithelial carbohydrates may predispose to GNB colonization by exposing binding sites for GNB.
重症疾病或应激可能促进革兰氏阴性菌(GNB)黏附并定植于呼吸道上皮的一种机制是改变上皮细胞表面碳水化合物。为了研究这种可能性,我们使用放射性标记的凝集素来定量完整颊黏膜和气管上皮上的碳水化合物水平。采用了一种GNB定植的大鼠模型,其中通过进行肾梗死来产生定植。比较了正常大鼠和肾梗死后48小时大鼠的颊黏膜和气管上皮表面碳水化合物水平。肾梗死动物的颊黏膜和气管上皮中唾液酸和岩藻糖含量减少,并且这些糖水平的降低与严重的口咽部GNB定植同时出现。梗死动物的气管结合1型菌毛GNB的能力是正常气管的三倍。应激后早期唾液酸和岩藻糖水平降低,我们推测上皮碳水化合物的改变可能通过暴露GNB的结合位点而使机体易发生GNB定植。