[Molecular mechanism for pathogenicity of Salmonella sp].

Inda Marcela Figueroa Ochoa, Antonio Verdugo Rodríguez
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Abstract

Salmonella is a Gram negative bacillus that behaves like a facultative intracellular pathogen. Its environment is the human and animal gastrointestinal tracts, it is never found like a normal microbiota. It is associated with gastrointestinal problems, septicaemic disease and abortion, due to its cellular invasion capacity and its intraphagocytic survival. Nowadays, it is known that Salmonella contains five pathogenicity islands. Several genes involved in the cellular invasion of nonphagocytic cells such as epithelial cells, apoptosis of macrophages, activation of routes of MAP kinases and transcription factors are located in centisome 63, constituting the pathogenicity island 1 (SPI-1). The SPI-2 and SPI-3 islands control the intracellular survival and replication. The SPI-4 island encodes a putative type I secretion system and its believed that it participates in the intracellular survival. Finally, the SPI-5 island encodes for factors involved in the fluid secretion and inflammatory reaction in the intestinal mucosa. Due to a coordinated and precise regulation of the Salmonella genes, it allows for adaptation to environmental changes that occur during an inflammatory process.

沙门氏菌致病性的分子机制
沙门氏菌是一种革兰氏阴性杆菌,表现得像兼性细胞内病原体。它的环境是人类和动物的胃肠道,它永远不会像正常的微生物群一样被发现。由于其细胞侵袭能力和吞噬细胞内存活,它与胃肠道问题、败血症和流产有关。如今,已知沙门氏菌含有5个致病性岛。参与上皮细胞等非吞噬细胞侵袭、巨噬细胞凋亡、MAP激酶和转录因子通路激活的几个基因位于63位,构成了致病岛1 (pathogenicity island 1, SPI-1)。SPI-2和SPI-3岛控制细胞内存活和复制。SPI-4岛编码一个假定的I型分泌系统,并被认为参与细胞内存活。最后,SPI-5岛编码参与肠粘膜液体分泌和炎症反应的因子。由于沙门氏菌基因的协调和精确调节,它允许适应炎症过程中发生的环境变化。
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