Enterococcus faecalis Infection Causes Inflammation, Intracellular Oxphos-Independent ROS Production, and DNA Damage in Human Gastric Cancer Cells

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Fältnamn	Indikatorer	Metadata
000		04208naa a2200409 4500
001		oai:lup.lub.lu.se:7611917a-31f9-4e2e-bf16-26db095c3726
003		SwePub
008		160401s2013 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://lup.lub.lu.se/record/39312272 URI
024	7	a https://doi.org/10.1371/journal.pone.00631472 DOI
040		a (SwePub)lu
041		a engb eng
042		9 SwePub
072	7	a art2 swepub-publicationtype
072	7	a ref2 swepub-contenttype
100	1	a Strickertsson, Jesper A. B.4 aut
245	1 0	a Enterococcus faecalis Infection Causes Inflammation, Intracellular Oxphos-Independent ROS Production, and DNA Damage in Human Gastric Cancer Cells
264		c 2013-04-30
264	1	b Public Library of Science (PLoS),c 2013
338		a electronic2 rdacarrier
520		a Background: Achlorhydria caused by e.g. atrophic gastritis allows for bacterial overgrowth, which induces chronic inflammation and damage to the mucosal cells of infected individuals driving gastric malignancies and cancer. Enterococcus faecalis (E. faecalis) can colonize achlohydric stomachs and we therefore wanted to study the impact of E. faecalis infection on inflammatory response, reactive oxygen species (ROS) formation, mitochondrial respiration, and mitochondrial genetic stability in gastric mucosal cells. Methods: To separate the changes induced by bacteria from those of the inflammatory cells we established an in vitro E. faecalis infection model system using the gastric carcinoma cell line MKN74. Total ROS and superoxide was measured by fluorescence microscopy. Cellular oxygen consumption was characterized non-invasively using XF24 microplate based respirometry. Gene expression was examined by microarray, and response pathways were identified by Gene Set Analysis (GSA). Selected gene transcripts were verified by quantitative real-time polymerase chain reaction (qRT-PCR). Mitochondrial mutations were determined by sequencing. Results: Infection of MKN74 cells with E. faecalis induced intracellular ROS production through a pathway independent of oxidative phosphorylation (oxphos). Furthermore, E. faecalis infection induced mitochondrial DNA instability. Following infection, genes coding for inflammatory response proteins were transcriptionally up-regulated while DNA damage repair and cell cycle control genes were down-regulated. Cell growth slowed down when infected with viable E. faecalis and responded in a dose dependent manner to E. faecalis lysate. Conclusions: Infection by E. faecalis induced an oxphos-independent intracellular ROS response and damaged the mitochondrial genome in gastric cell culture. Finally the bacteria induced an NF-kappa B inflammatory response as well as impaired DNA damage response and cell cycle control gene expression.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Mikrobiologi inom det medicinska området0 (SwePub)301092 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Microbiology in the medical area0 (SwePub)301092 hsv//eng
700	1	a Desler, Claus4 aut
700	1	a Martin-Bertelsen, Tomasu University of Copenhagen4 aut0 (Swepub:lu)thep-tme
700	1	a Machado, Ana Manuel Dantas4 aut
700	1	a Wadström, Torkelu Lund University,Lunds universitet,Avdelningen för medicinsk mikrobiologi,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Medical Microbiology,Department of Laboratory Medicine,Faculty of Medicine4 aut0 (Swepub:lu)mmb-twa
700	1	a Winther, Ole4 aut
700	1	a Rasmussen, Lene Juel4 aut
700	1	a Friis-Hansen, Lennart4 aut
710	2	a University of Copenhagenb Avdelningen för medicinsk mikrobiologi4 org
773	0	t PLoS ONEd : Public Library of Science (PLoS)g 8:4q 8:4x 1932-6203
856	4	u https://portal.research.lu.se/files/4184885/4145674x primaryx freey FULLTEXT
856	4	u http://dx.doi.org/10.1371/journal.pone.0063147x freey FULLTEXT
856	4	u https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0063147&type=printable
856	4 8	u https://lup.lub.lu.se/record/3931227
856	4 8	u https://doi.org/10.1371/journal.pone.0063147

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Av lärosätet: Lunds universitet

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