Kittana Hatem, Quintero-Villegas Maria I, Bindels Laure B, Gomes-Neto João Carlos, Schmaltz Robert J, Segura Munoz Rafael R, Cody Liz A, Moxley Rodney A, Hostetter Jesse, Hutkins Robert W, Ramer-Tait Amanda E
Department of Food Science and Technology, University of Nebraska-Lincoln, Lincoln, NE, USA.
School of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE, USA.
Microbiology (Reading). 2018 Feb;164(2):154-162. doi: 10.1099/mic.0.000593. Epub 2017 Dec 19.
Many enteric pathogens, including Salmonella and enteropathogenic and enterohemorrhagic Escherichia coli, express adhesins that recognize and bind to carbohydrate moieties expressed on epithelial cells. An attractive strategy for inhibiting bacterial adherence employs molecules that mimic these epithelial binding sites. Prebiotic oligosaccharides are non-digestible, fermentable fibres capable of modulating the gut microbiota. Moreover, they may act as molecular decoys that competitively inhibit adherence of pathogens to host cells. In particular, galactooligosaccharides (GOS) and other prebiotic fibres have been shown to inhibit pathogen adherence to epithelial cells in vitro. In the present study, we determined the ability of prophylactic GOS administration to reduce enteric pathogen adherence both in vitro and in vivo as well as protect against intestinal inflammation. GOS supplementation significantly reduced the adherence of the epithelial-adherent murine bacterial pathogen Citrobacter rodentium in a dose-dependent manner to the surface of epithelial cells in vitro. A 1- to 2-log reduction in bacterial adherence was observed at the lowest and highest doses tested, respectively. However, mouse studies revealed that treatment with GOS neither reduced the adherence of C. rodentium to the distal colon nor decreased its dissemination to systemic organs. Despite the absence of adherence inhibition, colonic disease scores for GOS-treated, C. rodentium-infected mice were significantly lower than those of untreated C. rodentium-infected animals (P=0.028). Together, these data suggest that GOS has a direct protective effect in ameliorating disease severity following C. rodentium infection through an anti-adherence-independent mechanism.
许多肠道病原体,包括沙门氏菌、肠致病性大肠杆菌和肠出血性大肠杆菌,都会表达能识别并结合上皮细胞上碳水化合物部分的黏附素。一种有吸引力的抑制细菌黏附的策略是使用模仿这些上皮细胞结合位点的分子。益生元低聚糖是能够调节肠道微生物群的不可消化、可发酵纤维。此外,它们可能充当分子诱饵,竞争性抑制病原体对宿主细胞的黏附。特别是,低聚半乳糖(GOS)和其他益生元纤维已被证明在体外能抑制病原体对上皮细胞的黏附。在本研究中,我们确定了预防性给予GOS在体外和体内降低肠道病原体黏附以及预防肠道炎症的能力。补充GOS以剂量依赖的方式显著降低了上皮黏附性鼠源细菌病原体鼠柠檬酸杆菌在体外对上皮细胞表面的黏附。在测试的最低和最高剂量下,分别观察到细菌黏附减少了1至2个对数。然而,小鼠研究表明,用GOS治疗既没有降低鼠柠檬酸杆菌对远端结肠的黏附,也没有减少其向全身器官的扩散。尽管没有黏附抑制作用,但用GOS治疗的、感染鼠柠檬酸杆菌的小鼠的结肠疾病评分显著低于未治疗的感染鼠柠檬酸杆菌的动物(P = 0.028)。总之,这些数据表明,GOS通过一种不依赖抗黏附的机制,在改善鼠柠檬酸杆菌感染后的疾病严重程度方面具有直接保护作用。