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抗脂多糖抗体可阻断产志贺毒素大肠杆菌对人肠上皮(亨勒407)细胞的黏附。

Antibodies to lipopolysaccharide block adherence of Shiga toxin-producing Escherichia coli to human intestinal epithelial (Henle 407) cells.

作者信息

Paton A W, Voss E, Manning P A, Paton J C

机构信息

Molecular Microbiology Unit, Women's and Children's Hospital, North Adelaide, S.A, 5006, Australia.

出版信息

Microb Pathog. 1998 Jan;24(1):57-63. doi: 10.1006/mpat.1997.0172.

Abstract

Shiga toxin-producing Escherichia coli (STEC) are a diverse group of organisms known to cause diarrhoea, haemorrhagic colitis and haemolytic uraemic syndrome (HUS) in humans. During the early stage of infection, numbers of STEC in the gut may be very high (of the order of 10(9)/g faeces), but as disease progresses, the numbers may drop rapidly such that STEC are undetectable within a week. Convalescent sera from patients recovering from HUS frequently contain high levels of antibody to E. coli lipopolysaccharide (LPS) of the infecting serotype, and it is possible that a local immune response to LPS contributes to elimination of the organism from the gut. We have recently demonstrated that STEC strains isolated from HUS cases have enhanced adherence to a human intestinal epithelial cell line (Henle 407) compared with STEC strains from non-human sources. In this study, we examined the capacity of STEC strains belonging to O-antigen types O111 and O157 to adhere to human intestinal epithelial (Henle 407) cells in the presence or absence of anti-LPS. Adherence was inhibited by up to 95% by anti-LPS of the homologous, but not heterologous serotype. This effect was not an artefact of serum bactericidal or agglutinating activity. Preincubation with purified homologous or heterologous LPS did not prevent adherence, suggesting that LPS was not acting as an adhesin per se. Nevertheless, these findings raise the possibility that oral administration of preparations containing anti-LPS may interfere with colonization of the human gut by STEC, and therefore could be of potential therapeutic value if administered early in the course of infection.

摘要

产志贺毒素大肠杆菌(STEC)是一类多样的微生物,已知可导致人类腹泻、出血性结肠炎和溶血尿毒综合征(HUS)。在感染早期,肠道中的STEC数量可能非常高(约为每克粪便10⁹个),但随着疾病进展,数量可能迅速下降,以至于在一周内无法检测到STEC。从HUS康复的患者的恢复期血清中经常含有高水平的针对感染血清型大肠杆菌脂多糖(LPS)的抗体,并且对LPS的局部免疫反应可能有助于从肠道中清除该微生物。我们最近证明,与非人类来源的STEC菌株相比,从HUS病例中分离出的STEC菌株对人肠上皮细胞系(Henle 407)的黏附增强。在本研究中,我们检测了属于O抗原类型O111和O157的STEC菌株在存在或不存在抗LPS的情况下与人肠上皮(Henle 407)细胞黏附的能力。同源血清型的抗LPS可将黏附抑制高达95%,而异源血清型则不能。这种效应不是血清杀菌或凝集活性的假象。用纯化的同源或异源LPS预孵育并不能阻止黏附,这表明LPS本身并不是一种黏附素。然而,这些发现增加了口服含抗LPS制剂可能干扰STEC在人肠道定植的可能性,因此如果在感染过程早期给药可能具有潜在的治疗价值。

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