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Atherosclerosis. 2017 Aug;263:177-183. doi: 10.1016/j.atherosclerosis.2017.06.016. Epub 2017 Jun 8.

Bacterial profile in human atherosclerotic plaques.

Author information

1
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Bruna Stråket 16, 41345 Gothenburg, Sweden.
2
Department of Public Health and Clinical Medicine, Umeå Stroke Centre, Umeå University, Umeå, Sweden; Department of Pharmacology and Clinical Neuroscience, Umeå University, Umeå, Sweden.
3
Department of Public Health and Clinical Medicine, Umeå Stroke Centre, Umeå University, Umeå, Sweden; Karolinska Institute Danderyds Hospital, Department of Clinical Sciences, Stockholm, Sweden.
4
Department of Surgical and Perioperative Sciences, Umeå University, Umeå, Sweden.
5
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Bruna Stråket 16, 41345 Gothenburg, Sweden. Electronic address: fredrik.backhed@wlab.gu.se.
6
The Wallenberg Laboratory, Department of Molecular and Clinical Medicine, University of Gothenburg, Bruna Stråket 16, 41345 Gothenburg, Sweden; Department of Clinical Physiology, Sahlgrenska University Hospital, Gothenburg, Sweden. Electronic address: Goran.Bergstrom@hjl.gu.se.

Abstract

BACKGROUND AND AIMS:

Several studies have confirmed the presence of bacterial DNA in atherosclerotic plaques, but its contribution to plaque stability and vulnerability is unclear. In this study, we investigated whether the bacterial plaque-profile differed between patients that were asymptomatic or symptomatic and whether there were local differences in the microbial composition within the plaque.

METHODS:

Plaques were removed by endarterectomy from asymptomatic and symptomatic patients and divided into three different regions known to show different histological vulnerability: A, upstream of the maximum stenosis; B, site for maximum stenosis; C, downstream of the maximum stenosis. Bacterial DNA composition in the plaques was determined by performing 454 pyrosequencing of the 16S rRNA genes, and total bacterial load was determined by qPCR.

RESULTS:

We confirmed the presence of bacterial DNA in the atherosclerotic plaque by qPCR analysis of the 16S rRNA gene but observed no difference (n.s.) in the amount between either asymptomatic and symptomatic patients or different plaque regions A, B and C. Unweighted UniFrac distance metric analysis revealed no distinct clustering of samples by patient group or plaque region. Operational taxonomic units (OTUs) from 5 different phyla were identified, with the majority of the OTUs belonging to Proteobacteria (48.3%) and Actinobacteria (40.2%). There was no difference between asymptomatic and symptomatic patients, or plaque regions, when analyzing the origin of DNA at phylum, family or OTU level (n.s.).

CONCLUSIONS:

There were no major differences in bacterial DNA amount or microbial composition between plaques from asymptomatic and symptomatic patients or between different plaque regions, suggesting that other factors are more important in determining plaque vulnerability.

KEYWORDS:

Atherosclerosis; Microbiota; Plaque

[Indexed for MEDLINE]

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