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Sialic Acid Metabolism and Systemic Pasteurellosis

机译：唾液酸代谢和全身巴氏杆菌病

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Pasteurella multocida subsp. multocida is a commensal and opportunistic pathogen of food animals, wildlife, and pets and a zoonotic cause of human infection arising from contacts with these animals. Here, an investigation of multiple serotype A strains demonstrated the occurrence of membrane sialyltransferase. Although P. multocida lacks the genes for the two earliest steps in de novo sialic acid synthesis, adding sialic acid to the growth medium resulted in uptake, activation, and subsequent transfer of sialic acid to a membrane acceptor resembling lipooligosaccharide. Two candidate-activating enzymes with homology to Escherichia coli cytidine 5′-monophospho-N-acetylneuraminate synthetase were overproduced as histidine-tagged polypeptides. The synthetase encoded by pm0187 was at least 37 times more active than the pm1710 gene product, suggesting pm0187 encodes the primary sialic acid cytidylyltransferase in P. multocida. A sialate aldolase (pm1715) mutant unable to initiate dissimilation of internalized sialic acid was not attenuated in the CD-1 mouse model of systemic pasteurellosis, indicating that the nutritional function of sialate catabolism is not required for systemic disease. In contrast, the attenuation of a sialate uptake-deficient mutant supports the essential role in pathogenesis of a sialylation mechanism that is dependent on an environmental (host) supply of sialic acid. The combined results provide the first direct evidence of sialylation by a precursor scavenging mechanism in pasteurellae and of a potential tripartite ATP-independent periplasmic sialate transporter in any species.
机译：多杀巴斯德氏菌子亚种。 multocida 是食用动物，野生动物和宠物的常见和机会病原体，是与这些动物接触而引起人感染的人畜共患病原因。在这里，对多种血清型A菌株的研究证实了膜唾液酸转移酶的发生。虽然 P。 multocida 缺乏从头唾液酸合成的两个最早步骤的基因，将唾液酸添加到生长培养基中会导致唾液酸的吸收，活化以及随后转移到类似于脂寡糖的膜受体上。与组氨酸标记的多肽过量生产了两种与大肠杆菌胞嘧啶核苷5'-单磷酸- N -乙酰神经氨酸合成酶具有同源性的候选酶。 pm0187编码的合成酶的活性至少是pm1710基因产物的37倍，这表明pm0187编码 P中的伯唾液酸胞嘧啶转移酶。多毛虫。在系统性巴氏杆菌病的CD-1小鼠模型中，无法激活唾液酸醛缩酶（pm1715）突变体无法启动内化唾液酸的异化作用，这表明系统性疾病不需要唾液酸分解代谢的营养功能。相反，唾液酸摄取不足突变体的衰减支持了依赖于环境（宿主）唾液酸供应的唾液酸化机制的发病机理中的重要作用。结合的结果提供了通过巴氏杆菌中的前体清除机制进行唾液酸化的第一个直接证据，以及任何物种中潜在的不依赖三方ATP的周质唾液酸转运蛋白。

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