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首页> 外文期刊>Infection and immunity >Intestinal Adherence of Vibrio cholerae Involves a Coordinated Interaction between Colonization Factor GbpA and Mucin
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Intestinal Adherence of Vibrio cholerae Involves a Coordinated Interaction between Colonization Factor GbpA and Mucin

机译：霍乱弧菌的肠黏附涉及定居因子GbpA和粘蛋白之间的协调相互作用。

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The chitin-binding protein GbpA of Vibrio cholerae has been recently described as a common adherence factor for chitin and intestinal surface. Using an isogenic in-frame gbpA deletion mutant, we first show that V. cholerae O1 El Tor interacts with mouse intestinal mucus quickly, using GbpA in a specific manner. The gbpA mutant strain showed a significant decrease in intestinal adherence, leading to less colonization and fluid accumulation in a mouse in vivo model. Purified recombinant GbpA (rGbpA) specifically bound to N-acetyl-d-glucosamine residues of intestinal mucin in a dose-dependent, saturable manner with a dissociation constant of 11.2 μM. Histopathology results from infected mouse intestine indicated that GbpA binding resulted in a time-dependent increase in mucus secretion. We found that rGbpA increased the production of intestinal secretory mucins (MUC2, MUC3, and MUC5AC) in HT-29 cells through upregulation of corresponding genes. The upregulation of MUC2 and MUC5AC genes was dependent on NF-κB nuclear translocation. Interestingly, mucin could also increase GbpA expression in V. cholerae in a dose-dependent manner. Thus, we propose that there is a coordinated interaction between GbpA and mucin to upregulate each other in a cooperative manner, leading to increased levels of expression of both of these interactive factors and ultimately allowing successful intestinal colonization and pathogenesis by V. cholerae.
机译：霍乱弧菌的几丁质结合蛋白GbpA最近被描述为几丁质和肠道表面的常见粘附因子。使用同基因的框内 gbpA 缺失突变体，我们首先显示了 V。霍乱弧菌O1 El Tor通过GbpA以特定方式快速与小鼠肠道粘液相互作用。在小鼠体内模型中， gbpA 突变株显示出肠粘连的显着降低，从而导致较少的定植和液体积聚。纯化的重组GbpA（rGbpA）以剂量依赖性，饱和方式与肠粘蛋白的 N -乙酰基-d-葡萄糖胺残基特异性结合，解离常数为11.2μM。感染小鼠肠道的组织病理学结果表明，GbpA结合导致粘液分泌随时间增加。我们发现rGbpA通过相应基因的上调增加了HT-29细胞中肠道分泌粘蛋白（MUC2，MUC3和MUC5AC）的产量。 MUC2 和 MUC5AC 基因的上调取决于NF-κB核易位。有趣的是，粘蛋白还可以增加 V中的GbpA表达。霍乱呈剂量依赖性。因此，我们建议在GbpA和粘蛋白之间存在协同相互作用，以协同方式相互上调，从而导致这两个相互作用因子的表达水平提高，并最终允许 V成功地在肠道中定植和致病。霍乱。

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