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Bacterial pathogens exploit normal h...

Monack, Denise Marie.

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Bacterial pathogens exploit normal host cell processes to cause gastrointestinal disease.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Bacterial pathogens exploit normal host cell processes to cause gastrointestinal disease./
Author:	Monack, Denise Marie.
Description:	167 p.
Notes:	Adviser: Stanley Falkow.
Contained By:	Dissertation Abstracts International63-01B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3038126
ISBN:	0493519203

Bacterial pathogens exploit normal host cell processes to cause gastrointestinal disease.
Monack, Denise Marie.

Bacterial pathogens exploit normal host cell processes to cause gastrointestinal disease. - 167 p.

Adviser: Stanley Falkow.

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

Many bacterial pathogens exploit normal host cell processes to cause disease. <italic>S. flexneri</italic>, a causative agent of gastrointestinal infections, exploits the normal host processes of motility and paracytophagy to spread intercellularly. My work has demonstrated that the addition of a single gene, <italic>icsA</italic>, which is sufficient for actin based motility, from <italic>S. flexneri</italic> into a non-pathogenic bacteria allows it to spread intercellularly. Thus, actin-based motility is sufficient for protrusion formation and uptake by neighboring cells.

ISBN: 0493519203Subjects--Topical Terms:

1017686
Biology, Cell.

Bacterial pathogens exploit normal host cell processes to cause gastrointestinal disease.
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020 $a 0493519203
035 $a (UnM)AAI3038126
035 $a AAI3038126
040 $a UnM $c UnM
100 1 $a Monack, Denise Marie. $3 1251226
245 1 0 $a Bacterial pathogens exploit normal host cell processes to cause gastrointestinal disease.
300 $a 167 p.
500 $a Adviser: Stanley Falkow.
500 $a Source: Dissertation Abstracts International, Volume: 63-01, Section: B, page: 0074.
502 $a Thesis (Ph.D.)--Stanford University, 2002.
520 $a Many bacterial pathogens exploit normal host cell processes to cause disease. <italic>S. flexneri</italic>, a causative agent of gastrointestinal infections, exploits the normal host processes of motility and paracytophagy to spread intercellularly. My work has demonstrated that the addition of a single gene, <italic>icsA</italic>, which is sufficient for actin based motility, from <italic>S. flexneri</italic> into a non-pathogenic bacteria allows it to spread intercellularly. Thus, actin-based motility is sufficient for protrusion formation and uptake by neighboring cells.
520 $a <italic>Salmonella</italic>, a causative agent of gastroenteritis and typhoid fever, exploits normal macrophage cell death pathways to cause apoptosis by injecting effector proteins into host cells. <italic>Salmonella typhimurium </italic>, induces a rapid cell death that requires the protein secretion apparatus encoded on <italic>Salmonella</italic> pathogenicity island 1, SPI1, to inject SipB into the host cytosol. SipB binds and activates the host protein caspase-1, a member of the pro-apoptotic caspase family of proteases, which leads to a rapid macrophage death. My research showed that <italic>S. typhimurium </italic> also triggers a delayed death that is dependent on SPI2 and caspase-1. Caspase-1 is unique among caspases because it also directly cleaves the proinflammatory cytokines Interleukin (IL)-1β and IL-18 to produce bioactive cytokines. To test the roles of caspase-1 and IL-1β in <italic>Salmonella</italic> infection, we infected mice that are deficient for these host proteins. I found that mice lacking caspase-1 or IL-1β had an oral <italic>S. typhimurium </italic> LD<sub>50</sub> that was 1000-fold or 30-fold higher than wild-type mice, respectively. There was a positive correlation between the frequency of TUNEL-positive nuclei, inflammation and <italic>S. typhimurium</italic> colonization of the gastrointestinal tract. Thus, caspase-1, which is both proapoptotic and proinflammatory, and IL-1β, which is responsible for eliciting a proinflammatory response, are essential for <italic>S. typhimurium </italic> to efficiently colonize the cecum and PP and subsequently cause systemic typhoid-like disease in mice. That bacterial pathogens, from those infecting plants to those infecting humans, use sophisticated molecular mechanisms to exploit host cell processes and host immune functions to cause disease inspires awe and gives us added respect for the adaptability of microorganisms.
590 $a School code: 0212.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0307
690 $a 0379
690 $a 0410
690 $a 0571
710 2 0 $a Stanford University. $3 754827
773 0 $t Dissertation Abstracts International $g 63-01B.
790 $a 0212
790 1 0 $a Falkow, Stanley, $e advisor
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3038126