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Role of SPI1 in Salmonella typhimuri...

Murray, Rose Ann.

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Role of SPI1 in Salmonella typhimurium pathogenesis.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Role of SPI1 in Salmonella typhimurium pathogenesis./
作者:	Murray, Rose Ann.
面頁冊數:	214 p.
附註:	Adviser: Catherine Lee.
Contained By:	Dissertation Abstracts International63-04B.
標題:	Biology, Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3051247
ISBN:	0493657797

Role of SPI1 in Salmonella typhimurium pathogenesis.
Murray, Rose Ann.

Role of SPI1 in Salmonella typhimurium pathogenesis. - 214 p.

Adviser: Catherine Lee.

Thesis (Ph.D.)--Harvard University, 2002.

<italic>Salmonella typhimurium</italic> causes a self-limiting gastroenteritis in humans but in mice it causes a systemic, typhoid-like disease. Following ingestion, bacteria colonize the intestinal tract, penetrate the intestinal epithelium and access systemic sites such as the spleen and liver through the lymphatic and blood circulation. Penetration of the intestinal wall is thought to be initiated by bacterial invasion of enterocytes and M cells. <italic> Salmonella</italic> is able to induce its own uptake into epithelial cells. Invasion is mediated by bacterial proteins called effectors that are secreted by a type III secretion system (TTSS). The components of the secretion machinery are encoded on a horizontally acquired fragment of DNA on the <italic>Salmonella </italic> chromosome, <italic>S&barbelow;almonella</italic> P&barbelow;athogenicity I&barbelow;sland 1&barbelow; (SPI1). Expression of the SPI1 TTSS is coordinately regulated by HilA, a transcriptional activator encoded on SPI1. In addition to playing a role in penetration of the intestinal wall, the SPI1 TTSS allows <italic>Salmonella</italic> to induce inflammation in a calf model of gastroenteritis, apoptosis of macrophages, and neutrophil transmigration across epithelial monolayers.

ISBN: 0493657797Subjects--Topical Terms:

1017734
Biology, Microbiology.

Role of SPI1 in Salmonella typhimurium pathogenesis.
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502 $a Thesis (Ph.D.)--Harvard University, 2002.
520 $a <italic>Salmonella typhimurium</italic> causes a self-limiting gastroenteritis in humans but in mice it causes a systemic, typhoid-like disease. Following ingestion, bacteria colonize the intestinal tract, penetrate the intestinal epithelium and access systemic sites such as the spleen and liver through the lymphatic and blood circulation. Penetration of the intestinal wall is thought to be initiated by bacterial invasion of enterocytes and M cells. <italic> Salmonella</italic> is able to induce its own uptake into epithelial cells. Invasion is mediated by bacterial proteins called effectors that are secreted by a type III secretion system (TTSS). The components of the secretion machinery are encoded on a horizontally acquired fragment of DNA on the <italic>Salmonella </italic> chromosome, <italic>S&barbelow;almonella</italic> P&barbelow;athogenicity I&barbelow;sland 1&barbelow; (SPI1). Expression of the SPI1 TTSS is coordinately regulated by HilA, a transcriptional activator encoded on SPI1. In addition to playing a role in penetration of the intestinal wall, the SPI1 TTSS allows <italic>Salmonella</italic> to induce inflammation in a calf model of gastroenteritis, apoptosis of macrophages, and neutrophil transmigration across epithelial monolayers.
520 $a I have studied the bacterial factors that mediated <italic>Salmonella </italic> pathogenesis using both the murine model of infection as well as a tissue culture model of inflammation. Using <italic>S. typhimurium</italic> strains containing mutations in SPI1, I have obtained results that challenge the prevailing ideas about the role SPI1 plays during infection. My findings suggest that SPI1 mutants have a reduced ability to colonize the intestine. Therefore, previous conclusions about SPI1 playing a direct role in invasion of the intestinal wall could be reinterpreted to mean that SPI1 promotes colonization of the ileum, which indirectly affects invasion of the intestinal wall. I also found that a strain missing the entirety of SPI1 was actually able to colonize the intestinal lumen and breach the intestinal wall. Based on my findings using the murine infection model, I have put forth a model that predicts the existence of a bacterial factor that elicits a host anti-bacterial response that is counteracted by SPI1 encoded factors.
520 $a I examined how <italic>S. typhimurium</italic> induces an immune response in a tissue culture model of inflammation. My studies showed that SipA, a SPI1 effector that induces neutrophil transmigration across epithelial monolayers, can be secreted by other TTSSs in <italic>Salmonella</italic>. In addition to SPI1, <italic>S. typhimurium</italic> has two other TTSSs: one encoded on a second pathogenicity island important for systemic disease (SPI2) and another encoded by flagellar genes, the flagellar basal body. Findings using the murine infection model suggest SipA plays an important role in early bacterial colonization of the intestine.
520 $a I have put forth a model that integrates our findings both in the murine infection model as well as in the tissue culture inflammation model. The SipA-dependent proinflammatory events promote early bacterial colonization of the intestine. This model pre dicts the existence of various bacterial factors that affect the secretion of bacterial effectors through different TTSSs. We believe this model expands our understanding of the complex interactions that occur within the bacteria and between the bacteria and its host over the course of infection.
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