宿主-肠道菌群的相互作用:粘液和甘露糖的作用

M. Romond, N. Chadli, T. Mitsuoka, C. Romond
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引用次数: 5

摘要

黏液和乳糖可能控制宿主与细菌的相互作用。在本研究中,我们用小鼠研究了它们各自的作用。通过比较糖蛋白SDS-PAGE图谱,分化了不同小鼠系(NC、CF1、BALB/c和C3H)的粘液。然后,我们试图确定各种双歧杆菌利用的肠道底物。首先,NC和CF1无菌小鼠接受了一种鼠种B. animalis的接种。细菌利用了几个CF1的糖基部分。glycocompounds。在NC小鼠中没有观察到这种广泛的降解。相比之下,NC和CF1。小鼠通过改变其高分子量粘蛋白的己糖胺组成来响应定植。然后测定了三种人结核菌(双歧杆菌、短结核菌和长结核菌)在体内降解C3H小鼠黏液的能力。两歧双歧杆菌广泛利用粘液中的糖蛋白,而长双歧杆菌和短双歧杆菌不能降解它们。然而,没有一种人类菌株导致肠粘蛋白修饰。菌株的来源似乎是控制宿主反应的一个因素。最后,研究了雌性乳糖对无菌、短芽孢杆菌相关和幼龄菌群相关C3H小鼠的影响。在前两个病例中,粘液成分几乎没有变化。在婴儿菌群相关小鼠中,检测到新的肠道糖蛋白和蛋白质,但细菌计数没有改变。宿主对乳糖的反应可能取决于一些未知的肠道细菌的植入。在母乳喂养的婴儿中,双歧杆菌的增殖很可能并不与直接的促乳糖作用相对应。但可能与乳糖引起的黏液改性有关。
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Host-Intestinal Microflora Interactions: Role of the Mucus and Gynolactose
Mucus and gynolactose might control host-Bjdobacterium interactions. Their respective roles were investigated in this study using gnotobiotic mice. By comparing glycoprotein SDS-PAGE profiles, mucus from various murine lines (NC, CF1, BALB/c and C3H) were differentiated. We attempted then to determine the intestinal substrates utilized by various bifidobacteria. First, NC and CF1 germfree mice received an inoculum of a murine species, B. animalis. Bacteria utilized the glycosyl fraction of several CF1. glycocompounds. No such extensive degradation was observed in NC mice. In constrast, both NC and CF1. mice responded to colonization by modifying hexosamine composition of their high molecular weight mucins. Three human species (B. bifidum, B. breve and B. longum) were then assayed for their in vivo capacity to degrade murine mucus from C3H mice. B. bifidum utilized extensively glycoproteins from the mucus, whereas B. longum and B. breve were unable to degrade them. However, none of the human strains led to intestinal mucins modification. Origin of the strains seemed to be a factor controlling the host response. Finally, gynolactose effect was investigated in germfree, B. breve-associated, and infant flora—associated C3H mice. Few modifications to mucus composition were noticed in the first two cases. In infant flora—associated mice, new intestinal glycoproteins and proteins were detected but bacterial counts were not changed. Host response to gynolactose might depend on the implantation of some unknown intestinal bacteria. It is likely that the proliferation of bifidobacteria shown in breast-fed infants does not correspond to a direct gynolactose promoting effect. But it is probably related to mucus modification induced by gynolactose.
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