東華大學圖書館 |

語系: 繁體中文

說明(常見問題)

回圖書館首頁

手機版館藏查詢

登入

回首頁

切換: 標籤 | MARC模式 | ISBD

Microbial-Host Interactions and Modu...

Donato, Kevin Andrew.

FindBook

Google Book

Amazon

博客來

Microbial-Host Interactions and Modulation of Epithelial Barrier Function: Pathogens to Probiotics.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Microbial-Host Interactions and Modulation of Epithelial Barrier Function: Pathogens to Probiotics./
作者:	Donato, Kevin Andrew.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2010,
面頁冊數:	178 p.
附註:	Source: Dissertation Abstracts International, Volume: 72-06, Section: B, page: 3206.
Contained By:	Dissertation Abstracts International72-06B.
標題:	Microbiology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR72131
ISBN:	9780494721315

Microbial-Host Interactions and Modulation of Epithelial Barrier Function: Pathogens to Probiotics.
Donato, Kevin Andrew.

Microbial-Host Interactions and Modulation of Epithelial Barrier Function: Pathogens to Probiotics. - Ann Arbor : ProQuest Dissertations & Theses, 2010 - 178 p.

Source: Dissertation Abstracts International, Volume: 72-06, Section: B, page: 3206.

Thesis (Ph.D.)--University of Toronto (Canada), 2010.

The epithelial cell layer that lines the intestine creates a barrier, largely mediated by the tight junction (TJ) apparatus, which serves as a first line of protection from the contents in the lumen containing an enormous number of microbes. Cellular microbiology, the study of microbial-host interactions, is used to describe mechanisms that play a role in the way epithelial cells regulate barrier properties in the context of bacterial colonization. The research in this thesis had three aims: (1) to characterize the effects of candidate pathogenic bacteria on the epithelial barrier, (2) to determine if a beneficial microbe (a probiotic bacterium) could ameliorate the deleterious effects of a pathogenic infection on this barrier, and (3) to extend the investigation of probiotic mechanisms in the context of pro-inflammatory cytokine-mediated barrier dysfunction.

ISBN: 9780494721315Subjects--Topical Terms:

536250
Microbiology.

Microbial-Host Interactions and Modulation of Epithelial Barrier Function: Pathogens to Probiotics.
LDR:04318nmm a2200325 4500 001 2126217
005 20171121071621.5
008 180830s2010 ||||||||||||||||| ||eng d
020 $a 9780494721315
035 $a (MiAaPQ)AAINR72131
035 $a AAINR72131
040 $a MiAaPQ $c MiAaPQ
100 1 $a Donato, Kevin Andrew. $3 3288307
245 1 0 $a Microbial-Host Interactions and Modulation of Epithelial Barrier Function: Pathogens to Probiotics.
260 1 $a Ann Arbor : $b ProQuest Dissertations & Theses, $c 2010
300 $a 178 p.
500 $a Source: Dissertation Abstracts International, Volume: 72-06, Section: B, page: 3206.
502 $a Thesis (Ph.D.)--University of Toronto (Canada), 2010.
520 $a The epithelial cell layer that lines the intestine creates a barrier, largely mediated by the tight junction (TJ) apparatus, which serves as a first line of protection from the contents in the lumen containing an enormous number of microbes. Cellular microbiology, the study of microbial-host interactions, is used to describe mechanisms that play a role in the way epithelial cells regulate barrier properties in the context of bacterial colonization. The research in this thesis had three aims: (1) to characterize the effects of candidate pathogenic bacteria on the epithelial barrier, (2) to determine if a beneficial microbe (a probiotic bacterium) could ameliorate the deleterious effects of a pathogenic infection on this barrier, and (3) to extend the investigation of probiotic mechanisms in the context of pro-inflammatory cytokine-mediated barrier dysfunction.
520 $a In the first part of this thesis, two undercharacterized bacterial species purported to cause diarrheal illness, Escherichia albertii and Hafnia alvei, were employed in a polarized epithelial infection model with outcome measures including transepithelial electrical resistance (TER), macromolecular permeability, TJ protein immunofluorescence staining, and immunoblotting. A well characterized pathogen, enterohemorrhagic Escherichia coli (EHEC), serotype O157:H7, was used as a positive control to demonstrate deleterious effects on TJs. All of the bacteria tested decreased TER, but the effects on TJs and TJ protein expression were specific to the bacterial strain tested and the epithelial model cell line used.
520 $a The second component of this thesis investigated how probiotics confer beneficial effects on epithelial barrier function. A probiotic bacterium, Lactobacillus rhamnosus GG (LGG), was employed to effectively block EHEC O157:H7 adherence to epithelial cells and prevent the ability of the pathogen to induce characteristic attaching-effacing lesions on epithelial cell surfaces. LGG ameliorated the pathogenic effects on barrier function normally induced by EHEC O157:H7, including prevention of decreased TER, increased permeability to a dextran probe, and rearrangement of tight junction architecture.
520 $a The third section elucidated the role of LGG in the prevention of barrier disruption due to pro-inflammatory cytokine stimuli (IFN-gamma and TNF-alpha). Using a polarized epithelial (Caco-2bbe) cell model, LGG treatment largely prevented cytokine-induced decreases in TER and TJ disruption. Furthermore, LGG suppressed the secretion of the chemokines interleukin-8 (CXCL-8) and eotaxin-1 (CCL-11), and the activation of NF-kappaB. Preliminary experimentation demonstrated a role for mitogen-activated protein kinases, with pharmacologic inhibition of extracellular signal related kinase (ERK-1/2) abolishing the protective effects of LGG.
520 $a Taken together, the findings presented in this thesis demonstrate how cellular microbiology models can be used to study host-microbial interactions, giving insight as to how the intestinal epithelium regulates barrier function; characterizing enteropathogenic candidates, and the diversity in responses to these bacteria that is dependent on both the bacterial strain and the epithelial cell line tested; and elucidating the mechanisms of probiotic action to reduce the deleterious effects of infection and inflammation.
590 $a School code: 0779.
650 4 $a Microbiology. $3 536250
650 4 $a Cellular biology. $3 3172791
690 $a 0410
690 $a 0379
710 2 $a University of Toronto (Canada). $3 1017674
773 0 $t Dissertation Abstracts International $g 72-06B.
790 $a 0779
791 $a Ph.D.
792 $a 2010
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=NR72131