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Effects of cell signalling on surviv...

University of Guelph (Canada).

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Effects of cell signalling on survival and virulence of Campylobacter jejuni.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Effects of cell signalling on survival and virulence of Campylobacter jejuni./
Author:	Moorhead, Sandra Maree.
Description:	194 p.
Notes:	Source: Dissertation Abstracts International, Volume: 70-03, Section: B, page: 1396.
Contained By:	Dissertation Abstracts International70-03B.
Subject:	Agriculture, Food Science and Technology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR47611
ISBN:	9780494476116

Effects of cell signalling on survival and virulence of Campylobacter jejuni.
Moorhead, Sandra Maree.

Effects of cell signalling on survival and virulence of Campylobacter jejuni. - 194 p.

Source: Dissertation Abstracts International, Volume: 70-03, Section: B, page: 1396.

Thesis (Ph.D.)--University of Guelph (Canada), 2009.

Campylobacter jejuni is the leading bacterial cause of food-borne illness worldwide. The regulation of survival and virulence mechanisms are not fully characterized in C. jejuni, however, the molecular basis for both survival and virulence traits of many bacteria is thought to involve cell-cell communication via autoinducers. There are three known autoinducer types allegedly produced by Gram-negative bacteria, designated AI-1, AI-2 and AI-3. This study investigated production of these molecules by C. jejuni, and then determined the effect of these signalling systems on selected survival and virulence characteristics. The AI-1 and AI-3 molecules and mimics investigated increased the transition rate to a viable but non culturable (VBNC) state, and decreased the organisms ability to form biofilms. These molecules and mimics were also involved to some degree in either up- or down-regulating the 5 virulence genes studied, as well as effecting an increase of interleukin-8 secretion in INT407 cells. Previous reports established that C. jejuni produces an AI-2 molecule via the luxS gene, so a luxS mutant was generated, and the above survival and virulence determinants examined. Complementation studies showed that the luxS mutation altered the wild-type phenotype, but these effects were not reversed when complemented with an AI-2 precursor. Finally, a range of defined as well as complex media and solutions were trialled to assess the ability to transform C. jejuni VBNC cells to a culturable state, but all were found to be unsatisfactory. In conclusion, C. jejuni may not produce classical AI-1 or AI-3 molecules, but is able to utilize these signals and mimics in gene regulation for both survival and virulence mechanisms. While C. jejuni produces an AI-2 molecule, this might be a byproduct of metabolism and not involved in gene regulation. It also appears that C. jejuni requires live animal models and specific hosts to transform from a VBNC state to a culturable state. These results give insight into cell-signalling utilization in survival and virulence mechanisms as well as having implications in developing new standard detection methods to replace the existing protocols which are not able to detect VBNC cells of C. jejuni .

ISBN: 9780494476116Subjects--Topical Terms:

1017813
Agriculture, Food Science and Technology.

Effects of cell signalling on survival and virulence of Campylobacter jejuni.
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500 $a Source: Dissertation Abstracts International, Volume: 70-03, Section: B, page: 1396.
502 $a Thesis (Ph.D.)--University of Guelph (Canada), 2009.
520 $a Campylobacter jejuni is the leading bacterial cause of food-borne illness worldwide. The regulation of survival and virulence mechanisms are not fully characterized in C. jejuni, however, the molecular basis for both survival and virulence traits of many bacteria is thought to involve cell-cell communication via autoinducers. There are three known autoinducer types allegedly produced by Gram-negative bacteria, designated AI-1, AI-2 and AI-3. This study investigated production of these molecules by C. jejuni, and then determined the effect of these signalling systems on selected survival and virulence characteristics. The AI-1 and AI-3 molecules and mimics investigated increased the transition rate to a viable but non culturable (VBNC) state, and decreased the organisms ability to form biofilms. These molecules and mimics were also involved to some degree in either up- or down-regulating the 5 virulence genes studied, as well as effecting an increase of interleukin-8 secretion in INT407 cells. Previous reports established that C. jejuni produces an AI-2 molecule via the luxS gene, so a luxS mutant was generated, and the above survival and virulence determinants examined. Complementation studies showed that the luxS mutation altered the wild-type phenotype, but these effects were not reversed when complemented with an AI-2 precursor. Finally, a range of defined as well as complex media and solutions were trialled to assess the ability to transform C. jejuni VBNC cells to a culturable state, but all were found to be unsatisfactory. In conclusion, C. jejuni may not produce classical AI-1 or AI-3 molecules, but is able to utilize these signals and mimics in gene regulation for both survival and virulence mechanisms. While C. jejuni produces an AI-2 molecule, this might be a byproduct of metabolism and not involved in gene regulation. It also appears that C. jejuni requires live animal models and specific hosts to transform from a VBNC state to a culturable state. These results give insight into cell-signalling utilization in survival and virulence mechanisms as well as having implications in developing new standard detection methods to replace the existing protocols which are not able to detect VBNC cells of C. jejuni .
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