Salmonella enterica serovar Gallinarum requires the Salmonella pathogenicity island 2 type III secretion system but not the Salmonella pathogenicity island 1 type III secretion system for virulence in chickens
Salmonella enterica serovar Gallinarum requires the Salmonella pathogenicity island 2 type III secretion system but not the Salmonella pathogenicity island 1 type III secretion system for virulence in chickens
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DOI：
10.1128/iai.69.9.5471-5476.2001
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发表时间：
2001-09-01
影响因子：
3.1
通讯作者：
Barrow, PA
中科院分区：
文献类型：
--
作者：
Jones, MA;Wigley, P;Barrow, PA
鸡沙门氏菌是一种宿主特有的血清型，在家禽和少数其他禽类中引起严重的全身性疾病，但在哺乳动物宿主中很少引起疾病。这种疾病的特异性主要是在网状内皮系统的水平上，但除了需要85kb的毒力质粒外，很少有毒力因子被描述。本工作通过对沙门氏菌致病性岛1(SPI-1)和SPI-2编码的III型分泌系统(TTSS)进行功能性突变，研究了这些致病岛在鸡群沙门氏菌与禽类细胞相互作用中的作用，以及这些致病岛在鸡的致病力中的作用。SPI-1突变体在体外对禽类细胞的侵袭力降低，但不影响其在鸡巨噬细胞内的存留能力。相比之下，SPI-2突变体在非吞噬细胞中是完全侵袭的，但在巨噬细胞中不能持续存在。在鸡感染中，SPI-2突变株表现出弱毒力，而SPI-1突变株则显示出完全的毒力。在口腔感染中，在脾或肝脏中没有观察到SPI-2突变体，在静脉接种后，它很快就从这些部位被清除。鸡沙门氏菌的毒力需要SPI-2功能，主要是通过促进巨噬细胞内的存活，允许网状内皮系统内的增殖，但这并不排除SPI-2参与从肠道到脾和肝脏的摄取。SPI-1对鸡沙门氏菌的毒力和在宿主中的存活几乎没有影响。
Salmonella enterica serovar Gallinarum is a host-specific serotype that causes the severe systemic disease fowl typhoid in domestic poultry and a narrow range of other avian species but rarely causes disease in mammalian hosts. Specificity of the disease is primarily at the level of the reticuloendothelial system, but few virulence factors have been described other than the requirement for an 85-kb virulence plasmid. In this work, by making functional mutations in the type III secretion systems (TTSS) encoded by Salmonella pathogenicity island 1 (SPI-1) and SPI-2, we investigated the role of these pathogenicity islands in interactions between Salmonella serovar Gallinarum and avian cells in vitro and the role of these pathogenicity islands in virulence in chickens. The SPI-1 mutant showed decreased invasiveness into avian cells in vitro but was unaffected in its ability to persist within chicken macrophages. In contrast the SPI-2 mutant was fully invasive in nonphagocytic cells but failed to persist in macrophages. In chicken infections the SPI-2 mutant was attenuated while the SPI-1 mutant showed full virulence. In oral infections the SPI-2 mutant was not observed in the spleen or liver, and following intravenous inoculation it was cleared rapidly from these sites. SPI-2 function is required by Salmonella serovar Gallinarum for virulence, primarily through promoting survival within macrophages allowing multiplication within the reticuloendothelial system, but this does not preclude the involvement of SPI-2 in uptake from the gut to the spleen and liver. SPI-1 appears to have little effect on virulence and survival of Salmonella serovar Gallinarum in the host.