Kingsley Robert A, Humphries Andrea D, Weening Eric H, De Zoete Marcel R, Winter Sebastian, Papaconstantinopoulou Anastasia, Dougan Gordon, Bäumler Andreas J
Department of Medical Microbiology and Immunology, College of Medicine, Texas A&M University System Health Science Center, College Station 77843-1114, USA.
Infect Immun. 2003 Feb;71(2):629-40. doi: 10.1128/IAI.71.2.629-640.2003.
The shdA gene is carried on a 25-kb genetic island at centisome 54 (CS54 island) of the Salmonella enterica serotype Typhimurium chromosome. In addition to shdA, the CS54 island of Salmonella serotype Typhimurium strain LT2 contains four open reading frames designated ratA, ratB, sivI, and sivH. DNA hybridization analysis revealed that the CS54 island is comprised of two regions with distinct phylogenetic distribution within the genus Salmonella. Homologues of shdA and ratB were detected only in serotypes of Salmonella enterica subsp. I. In contrast, sequences hybridizing with ratA, sivI, and sivH were present in S. enterica subsp. II and S. bongori in addition to S. enterica subsp. I. Deletion of the ratA and sivI genes did not alter the ability of Salmonella serotype Typhimurium to colonize the organs of mice. Insertional inactivation of the sivH gene resulted in defective colonization of the Peyer's patches of the terminal ileum but normal colonization of the cecum, mesenteric lymph nodes, and spleen. Deletion of the shdA gene resulted in decreased colonization of the cecum and Peyer's patches of the terminal ileum and colonization to a lesser degree in the mesenteric lymph nodes and spleen 5 days post-oral inoculation of mice. A strain containing a deletion in the ratB gene exhibited a defect for the colonization of the cecum but not of the Peyer's patches, mesenteric lymph nodes, and spleen. The shdA and ratB deletion strains exhibited a shedding defect in mice, whereas the sivH deletion strain was shed at numbers similar to the wild type. These data suggest that colonization of the murine cecum is required for efficient fecal shedding in mice.
shdA基因位于鼠伤寒沙门氏菌染色体54厘摩(CS54岛)处一个25千碱基的遗传岛上。除shdA外,鼠伤寒沙门氏菌LT2菌株的CS54岛还包含四个开放阅读框,分别命名为ratA、ratB、sivI和sivH。DNA杂交分析表明,CS54岛由沙门氏菌属内系统发育分布不同的两个区域组成。仅在肠炎沙门氏菌亚种I的血清型中检测到shdA和ratB的同源物。相反,除肠炎沙门氏菌亚种I外,与ratA、sivI和sivH杂交的序列还存在于肠炎沙门氏菌亚种II和邦戈尔沙门氏菌中。删除ratA和sivI基因不会改变鼠伤寒沙门氏菌在小鼠器官中定殖的能力。sivH基因的插入失活导致回肠末端派尔集合淋巴结定殖缺陷,但盲肠、肠系膜淋巴结和脾脏定殖正常。删除shdA基因导致盲肠和回肠末端派尔集合淋巴结定殖减少,口服接种小鼠5天后,肠系膜淋巴结和脾脏的定殖程度较低。含有ratB基因缺失的菌株在盲肠定殖方面存在缺陷,但在派尔集合淋巴结、肠系膜淋巴结和脾脏定殖方面没有缺陷。shdA和ratB缺失菌株在小鼠中表现出粪便排出缺陷,而sivH缺失菌株的排出数量与野生型相似。这些数据表明,小鼠盲肠的定殖是小鼠有效粪便排出所必需的。