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Host signaling response to adhesion ...

Gann, Reed N.

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Host signaling response to adhesion of Bifidobacterium infantis.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Host signaling response to adhesion of Bifidobacterium infantis./
Author:	Gann, Reed N.
Description:	132 p.
Notes:	Source: Masters Abstracts International, Volume: 48-05, page: .
Contained By:	Masters Abstracts International48-05.
Subject:	Biology, Molecular. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1475179
ISBN:	9781109723380

Host signaling response to adhesion of Bifidobacterium infantis.
Gann, Reed N.

Host signaling response to adhesion of Bifidobacterium infantis. - 132 p.

Source: Masters Abstracts International, Volume: 48-05, page: .

Thesis (M.S.)--Utah State University, 2010.

Investigations of the molecular binding partners of the probiotic bacterium Bifidobacterium longum subspecies infantis ( B. infantis) and the pathogen Salmonella enterica subspecies enterica serovar Typhimurium LT2 (Salmonella ser. Typhimurium) found that these two very different bacteria bind gangliosides. However, these organisms lead to completely different host health outcomes when present in the gut. B. infantis is the founding microbial population in the intestinal tract of breast-fed infants. S. typhimurium is the most important foodborne pathogen that results in humans. This study used an in vitro gut epithelial cell model to examine the host cellular response to adhesion of B. infantis, which led to an increase in intestinal epithelium survival. This observation led to a series of experiments to elucidate the pathway for host signaling initiated by adherence of B. infantis to the host membrane to explain the increase in host cell survival. B. infantis adhesion induced significant (q≤0.05) differential expression of 208 host genes. These genes were associated with increased broad mechanisms of cell survival that included BIRC3, TNFAIP3, and SERPINB9. We hypothesized that a biochemical link existed between the host membrane adhesion protein and the increase in cell survival, mediated via AKT. We tested this hypothesis to demonstrate that B. infantis interaction initiated signal transduction using G-proteins via phosphorylation of AKT and induced production of the BIRC3, TNFAIP3, and SERPINB9. This study discovered adhesion of B. infantis initiated activation of AKT via phosphorylation of both Ser473 and Thr308, which results in increased cell survival.

ISBN: 9781109723380Subjects--Topical Terms:

1017719
Biology, Molecular.

Host signaling response to adhesion of Bifidobacterium infantis.
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100 1 $a Gann, Reed N. $3 1669131
245 1 0 $a Host signaling response to adhesion of Bifidobacterium infantis.
300 $a 132 p.
500 $a Source: Masters Abstracts International, Volume: 48-05, page: .
500 $a Advisers: Daryll D. DeWald; Bart C. Weimer.
502 $a Thesis (M.S.)--Utah State University, 2010.
520 $a Investigations of the molecular binding partners of the probiotic bacterium Bifidobacterium longum subspecies infantis ( B. infantis) and the pathogen Salmonella enterica subspecies enterica serovar Typhimurium LT2 (Salmonella ser. Typhimurium) found that these two very different bacteria bind gangliosides. However, these organisms lead to completely different host health outcomes when present in the gut. B. infantis is the founding microbial population in the intestinal tract of breast-fed infants. S. typhimurium is the most important foodborne pathogen that results in humans. This study used an in vitro gut epithelial cell model to examine the host cellular response to adhesion of B. infantis, which led to an increase in intestinal epithelium survival. This observation led to a series of experiments to elucidate the pathway for host signaling initiated by adherence of B. infantis to the host membrane to explain the increase in host cell survival. B. infantis adhesion induced significant (q≤0.05) differential expression of 208 host genes. These genes were associated with increased broad mechanisms of cell survival that included BIRC3, TNFAIP3, and SERPINB9. We hypothesized that a biochemical link existed between the host membrane adhesion protein and the increase in cell survival, mediated via AKT. We tested this hypothesis to demonstrate that B. infantis interaction initiated signal transduction using G-proteins via phosphorylation of AKT and induced production of the BIRC3, TNFAIP3, and SERPINB9. This study discovered adhesion of B. infantis initiated activation of AKT via phosphorylation of both Ser473 and Thr308, which results in increased cell survival.
590 $a School code: 0241.
650 4 $a Biology, Molecular. $3 1017719
650 4 $a Biology, Microbiology. $3 1017734
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710 2 $a Utah State University. $b Biology. $3 1064589
773 0 $t Masters Abstracts International $g 48-05.
790 1 0 $a DeWald, Daryll D., $e advisor
790 1 0 $a Weimer, Bart C., $e advisor
790 1 0 $a Hevel, Joane $e committee member
790 $a 0241
791 $a M.S.
792 $a 2010
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=1475179