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Bacterial infection and atheroslcero...

Lanter, Bernard Benjamin.

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Bacterial infection and atheroslcerosis: Investigating the relationship between atherosclerosis, biofilm infections and the battle for iron.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Bacterial infection and atheroslcerosis: Investigating the relationship between atherosclerosis, biofilm infections and the battle for iron./
Author:	Lanter, Bernard Benjamin.
Description:	176 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-02(E), Section: B.
Contained By:	Dissertation Abstracts International77-02B(E).
Subject:	Microbiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3729333
ISBN:	9781339151045

Bacterial infection and atheroslcerosis: Investigating the relationship between atherosclerosis, biofilm infections and the battle for iron.
Lanter, Bernard Benjamin.

Bacterial infection and atheroslcerosis: Investigating the relationship between atherosclerosis, biofilm infections and the battle for iron. - 176 p.

Source: Dissertation Abstracts International, Volume: 77-02(E), Section: B.

Thesis (Ph.D.)--State University of New York at Binghamton, 2015.

In this dissertation, out of 15 human atherosclerotic carotid artery explants that were examined for the presence of bacterial 16S-rDNA, all tested positive for the presence of eubacterial 16S-rDNA, 6 tested positive for Pseudomonas sp. 16S-rDNA, and 4 tested positive for Propionibacterium sp. 16S-rDNA. Density gradient gel electrophoresis of 5 of the 15 samples revealed 10 or more distinct 16S-rDNA gene sequences in each sample, indicating a multi-species infection. An additional 10 atherosclerotic carotid arteries were screened for viable bacteria recoverable in culture, and P. acnes was one among 10 bacterial species recovered. To visualize the presence and location of the bacterial cells within atherosclerotic plaques, five of the original samples and 5 new samples were probed for eubacterial 16S-rDNA using fluorescence in situ hybridization (FISH). All probed samples contained bound probe indicating the presence of microcolonies, while 4 out of 5 samples were shown to be positive for bound P. acnes 23S-rDNA probe. Biofilms of P. aeruginosa PA01, P. acnes VP1 and P. acnes hdn1 grown in the presence of physiologically relevant levels of iron-bound transferrin were induced to disperse upon the addition of physiologically relevant levels of norepinephrine in vitro due to increased free iron. Biofilms induced to disperse by addition of free iron had higher lipolytic and proteolytic extracellular enzyme activity than un-induced cells, and showed increased transcript abundance for the triacylglycerol lipases PPA2105 and PPA1796, and hyaluronate lyase PPA380. Lipase, gelatinase and collagenase activity in supernatant liquids from P. acnes VP1 and hdn-1 biofilms were found to be higher than the activity in supernatant liquids from their respective planktonic counterparts. Transcript abundance of PPA1796, PPA2105 and the protease PPA0598 was >2-fold upregulated in VP1 and hdn-1 biofilm cells in relation to planktonic cells. These results demonstrated human atherosclerotic carotid arteries contain viable bacterial species, which appear to be present within plaques and tissues as biofilms. These biofilms may contribute to the pathogenesis of atherosclerosis through tissue degradation. In this study a potential mechanism was found that links the levels of the catechol hormone norepinephrine to biofilm dispersion, possibly resulting in increased damage to the surrounding tissues.

ISBN: 9781339151045Subjects--Topical Terms:

536250
Microbiology.

Bacterial infection and atheroslcerosis: Investigating the relationship between atherosclerosis, biofilm infections and the battle for iron.
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245 1 0 $a Bacterial infection and atheroslcerosis: Investigating the relationship between atherosclerosis, biofilm infections and the battle for iron.
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520 $a In this dissertation, out of 15 human atherosclerotic carotid artery explants that were examined for the presence of bacterial 16S-rDNA, all tested positive for the presence of eubacterial 16S-rDNA, 6 tested positive for Pseudomonas sp. 16S-rDNA, and 4 tested positive for Propionibacterium sp. 16S-rDNA. Density gradient gel electrophoresis of 5 of the 15 samples revealed 10 or more distinct 16S-rDNA gene sequences in each sample, indicating a multi-species infection. An additional 10 atherosclerotic carotid arteries were screened for viable bacteria recoverable in culture, and P. acnes was one among 10 bacterial species recovered. To visualize the presence and location of the bacterial cells within atherosclerotic plaques, five of the original samples and 5 new samples were probed for eubacterial 16S-rDNA using fluorescence in situ hybridization (FISH). All probed samples contained bound probe indicating the presence of microcolonies, while 4 out of 5 samples were shown to be positive for bound P. acnes 23S-rDNA probe. Biofilms of P. aeruginosa PA01, P. acnes VP1 and P. acnes hdn1 grown in the presence of physiologically relevant levels of iron-bound transferrin were induced to disperse upon the addition of physiologically relevant levels of norepinephrine in vitro due to increased free iron. Biofilms induced to disperse by addition of free iron had higher lipolytic and proteolytic extracellular enzyme activity than un-induced cells, and showed increased transcript abundance for the triacylglycerol lipases PPA2105 and PPA1796, and hyaluronate lyase PPA380. Lipase, gelatinase and collagenase activity in supernatant liquids from P. acnes VP1 and hdn-1 biofilms were found to be higher than the activity in supernatant liquids from their respective planktonic counterparts. Transcript abundance of PPA1796, PPA2105 and the protease PPA0598 was >2-fold upregulated in VP1 and hdn-1 biofilm cells in relation to planktonic cells. These results demonstrated human atherosclerotic carotid arteries contain viable bacterial species, which appear to be present within plaques and tissues as biofilms. These biofilms may contribute to the pathogenesis of atherosclerosis through tissue degradation. In this study a potential mechanism was found that links the levels of the catechol hormone norepinephrine to biofilm dispersion, possibly resulting in increased damage to the surrounding tissues.
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