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肠炎沙门氏菌肠炎血清型在鸡盲肠的定殖需要HilA调控蛋白。

Salmonella enterica serovar Enteritidis colonization of the chicken caecum requires the HilA regulatory protein.

作者信息

Bohez Lotte, Ducatelle Richard, Pasmans Frank, Botteldoorn Nadine, Haesebrouck Freddy, Van Immerseel Filip

机构信息

Department of Pathology, Bacteriology and Avian Diseases, Research Group Veterinary Public Health and Zoonoses, Faculty of Veterinary Medicine, Ghent University, Salisburylaan 133, B-9820 Merelbeke, Belgium.

出版信息

Vet Microbiol. 2006 Aug 25;116(1-3):202-10. doi: 10.1016/j.vetmic.2006.03.007. Epub 2006 Apr 27.

Abstract

Invasion of Salmonella into intestinal epithelial cells is believed to be essential for the pathogenesis of Salmonella infections. Invasion is mediated by genes located on the Salmonella pathogenicity Island I (SPI-1), which are needed for assembling a type three secretion system, that mediates injection of bacterial proteins into the cytosol of epithelial cells, resulting in cytoskeletal rearrangements and as a consequence invasion. HilA is the key regulator of the Salmonella Pathogenicity Island I. To assess the role of hilA in colonization of gut and internal organs in poultry, animals were infected with 10(8) CFU of a delta hilA mutant of S. Enteritidis and its parent strain at day of hatch. Very low numbers of delta hilA mutant strain were able to colonize the internal organs shortly after infection, but they were not eliminated from internal organs at 4 weeks post-infection. At that time, the colonization level of the wild type bacteria in internal organs was decreased to the same low level compared with delta hilA mutant strain bacteria. Shedding of the delta hilA mutant strain and colonization of the caeca was seriously decreased relative to the parent strain starting from Day 5 post-infection. At 4 weeks post-infection, the delta hilA mutant strain was more or less eliminated from the chicken gut, while the parent strain was still shed to a high level and colonized the caeca to a high extent (more than 10(7) CFU/g). It is concluded that hilA is involved in long-term shedding and colonization of S. Enteritidis in the chicken caeca.

摘要

沙门氏菌侵入肠道上皮细胞被认为是沙门氏菌感染发病机制的关键环节。这种侵入由位于沙门氏菌致病岛I(SPI-1)上的基因介导,这些基因对于组装三型分泌系统是必需的,该系统介导将细菌蛋白注入上皮细胞的细胞质中,导致细胞骨架重排,进而引发侵入。HilA是沙门氏菌致病岛I的关键调节因子。为了评估hilA在家禽肠道和内脏定植中的作用,在孵化当天用10⁸CFU肠炎沙门氏菌的hilA缺失突变株及其亲本菌株感染动物。感染后不久,极少量的hilA缺失突变株能够在内脏定植,但在感染后4周它们并未从内脏中被清除。此时,与hilA缺失突变株相比,野生型细菌在内脏中的定植水平降至相同的低水平。从感染后第5天开始,hilA缺失突变株的排出以及盲肠的定植相对于亲本菌株严重减少。在感染后4周,hilA缺失突变株或多或少从鸡肠道中被清除,而亲本菌株仍大量排出并在盲肠中高度定植(超过10⁷CFU/g)。结论是hilA参与肠炎沙门氏菌在鸡盲肠中的长期排出和定植。

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