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纳米唾液酸酶有助于梭状芽孢杆菌 CP56 型 G 菌株在体外表达毒素和与宿主细胞结合。

NanI sialidase contributes to toxin expression and host cell binding of Clostridium perfringens type G strain CP56 in vitro.

机构信息

Livestock Gut Health Team (LiGHT) Ghent, Department of Pathobiology, Pharmacology and Zoological Medicine, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, Merelbeke, Belgium.

Evonik Operations GmbH, Division Nutrition & Care - Animal Nutrition, 33790, Halle, Westfalen, Germany.

出版信息

Vet Microbiol. 2022 Mar;266:109371. doi: 10.1016/j.vetmic.2022.109371. Epub 2022 Feb 11.

Abstract

Necrotic enteritis, caused by NetB producing Clostridium perfringens type G strains, is a globally important poultry disease. An initial step in the pathogenesis of necrotic enteritis is the colonization and degradation of the intestinal mucus layer, a process in which C. perfringens sialidases - such as NanI sialidase - may play an important role. Sialidases cleave terminal sialic acid from complex carbohydrates on glycoconjugates, such as mucins. This study shows that NE-associated C. perfringens strain CP56 is able to use sialic acid (Neu5Ac) as a carbon source for bacterial growth. It is shown that supplementation of Neu5Ac in the growth medium does not only induce the production of extracellular sialidases of strain CP56, but also increases the production of both alpha toxin and NetB toxin. Moreover, it was found that pre-treating avian hepatocellular carcinoma cells (LMH cells) with the recombinant NanI sialidase increases the adherence of C. perfringens type G strain CP56 to these cells. As such, the data suggest an important role for sialidases in the pathogenesis of the disease.

摘要

坏死性肠炎是由产生 NetB 的 G 型产气荚膜梭菌引起的一种全球性重要家禽疾病。坏死性肠炎发病机制的初始步骤是肠道黏液层的定植和降解,产气荚膜梭菌唾液酸酶(如 NanI 唾液酸酶)在此过程中可能发挥重要作用。唾液酸酶从糖缀合物(如粘蛋白)上的复杂碳水化合物中切割末端唾液酸。本研究表明,与 NE 相关的 C. perfringens 菌株 CP56 能够将唾液酸(Neu5Ac)用作细菌生长的碳源。结果表明,在生长培养基中添加 Neu5Ac 不仅诱导 CP56 菌株的细胞外唾液酸酶的产生,而且还增加了 alpha 毒素和 NetB 毒素的产生。此外,研究发现,用重组 NanI 唾液酸酶预处理禽肝癌细胞(LMH 细胞)会增加 G 型产气荚膜梭菌 CP56 菌株对这些细胞的黏附。因此,数据表明唾液酸酶在疾病发病机制中起重要作用。

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