Moran A P
Department of Microbiology, University College, Galway, Ireland.
Aliment Pharmacol Ther. 1996 Apr;10 Suppl 1:39-50. doi: 10.1046/j.1365-2036.1996.22164004.x.
The present review describes the structure, attributes and properties of Helicobacter pylori lipopolysaccharides (LPS), and their potential role in pathogenesis. Although possessing certain attributes similar to those of LPS of other Gram-negative bacteria, H. pylori LPS possess unique biological properties. H. pylori LPS has, in general, low immunological activity and this property may aid the persistence of infection. The O-specific chain of the LPS mimics Lewis blood group antigens in structure. As these antigens are present in the gastric mucosa, the expression of Lewis antigens on the bacterial surface may camouflage the bacterium and aid survival of H. pylori. Alternatively, since autoantibodies against human antral gastric mucosa have been observed in H. pylori-positive patients, the relevance of LPS in the development of autoimmunity in H. pylori-associated disease requires further investigation. H. pylori LPS in part mediates the binding of the bacterium to laminin, and interferes with gastric cell receptor-laminin interaction, thereby potentially contributing to the loss of mucosal integrity. In vitro observations of inhibition of sulphated mucin synthesis and stimulation of pepsinogen secretion by LPS suggest new mechanisms for H. pylori-induced mucosal damage. Nevertheless, further in vivo studies are required to support their pathogenic role.
本综述描述了幽门螺杆菌脂多糖（LPS）的结构、特性和属性，以及它们在发病机制中的潜在作用。尽管幽门螺杆菌LPS具有某些与其他革兰氏阴性菌LPS相似的特性，但它具有独特的生物学特性。一般来说，幽门螺杆菌LPS的免疫活性较低，这一特性可能有助于感染的持续存在。LPS的O-特异性链在结构上模拟Lewis血型抗原。由于这些抗原存在于胃黏膜中，细菌表面Lewis抗原的表达可能会掩盖细菌，有助于幽门螺杆菌的存活。另外，由于在幽门螺杆菌阳性患者中观察到针对人胃窦黏膜的自身抗体，LPS在幽门螺杆菌相关疾病自身免疫发展中的相关性需要进一步研究。幽门螺杆菌LPS部分介导细菌与层粘连蛋白的结合，并干扰胃细胞受体与层粘连蛋白的相互作用，从而可能导致黏膜完整性的丧失。LPS抑制硫酸化粘蛋白合成和刺激胃蛋白酶原分泌的体外观察结果提示了幽门螺杆菌诱导黏膜损伤的新机制。然而，需要进一步的体内研究来支持它们的致病作用。
