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Demirel, Isak
Publications (10 of 28) Show all publications
Klarström-Engström, K., Zhang, B. & Demirel, I. (2019). Human renal fibroblasts are strong immunomobilizers during a urinary tract infection mediated by uropathogenic Escherichia coli. Scientific Reports, 9(1), Article ID 2296.
Open this publication in new window or tab >>Human renal fibroblasts are strong immunomobilizers during a urinary tract infection mediated by uropathogenic Escherichia coli
2019 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 9, no 1, article id 2296Article in journal (Refereed) Published
Abstract [en]

To prevent the onset of urosepsis and reduce mortality, a better understanding of how uropathogenic Escherichia coli (UPEC) manages to infiltrate the bloodstream through the kidneys is needed. The present study elucidates if human renal interstitial fibroblasts are part of the immune response limiting a UPEC infection, or if UPEC has the ability to modulate the fibroblasts for their own gain. Microarray results showed that upregulated genes were associated with an activated immune response. We also found that chemokines released from renal fibroblasts upon a UPEC infection could be mediated by LPS and triacylated lipoproteins activating the TLR2/1, TLR4, MAPK, NF-κB and PKC signaling pathways. Furthermore, UPEC was also shown to be able to adhere and invade renal fibroblasts, mediated by the P-fimbriae. Furthermore, it was found that renal fibroblasts were more immunoreactive than renal epithelial cells upon a UPEC infection. However, both renal fibroblasts and epithelial cells were equally efficient at inducing neutrophil migration. In conclusion, we have found that human renal fibroblasts can sense UPEC and mobilize a host response with neutrophil migration. This suggests that renal fibroblasts are not only structural cells that produce and regulate the extracellular matrix, but also highly immunoreactive cells.

Place, publisher, year, edition, pages
Nature Publishing Group, 2019
National Category
Immunology
Identifiers
urn:nbn:se:oru:diva-72784 (URN)10.1038/s41598-019-38691-8 (DOI)000459092800066 ()30783129 (PubMedID)2-s2.0-85061794911 (Scopus ID)
Note

Funding Agencies:

Research Committee of Örebro County Council  

Faculty of Medicine and Health at Örebro University 

Available from: 2019-02-26 Created: 2019-02-26 Last updated: 2019-06-19Bibliographically approved
Lindblad, A., Persson, K. & Demirel, I. (2019). IL-1RA is part of the inflammasome-regulated immune response in bladder epithelial cells and influences colonization of uropathogenic E. coli. Cytokine, 123, Article ID 154772.
Open this publication in new window or tab >>IL-1RA is part of the inflammasome-regulated immune response in bladder epithelial cells and influences colonization of uropathogenic E. coli
2019 (English)In: Cytokine, ISSN 1043-4666, E-ISSN 1096-0023, Vol. 123, article id 154772Article in journal (Refereed) Epub ahead of print
Abstract [en]

The NLRP3 inflammasome, IL-1β release and pyroptosis (cell lysis) have recently been proposed to be essential for the progression of urinary tract infection (UTI) and elimination of intracellular bacterial niches. However, the effects of IL-1R antagonist (IL-1RA) on immune responses during UTI, except for its ability to disrupt IL-1β signalling, are not well understood. The aim of this study was to investigate the role of IL-1RA in UPEC colonization of bladder epithelial cells and the subsequent host inflammatory response. Human bladder epithelial cells (5637) and CRISPR/Cas9 generated NLRP3 and caspase-1 knockdown cells and IL-1RA knockout cells were stimulated with the UPEC isolate CFT073. The results showed that the UPEC virulence factor α-hemolysin is essential for IL-1RA release, and that the inflammasome-associated proteins caspase-1 and NLRP3 affect the release of IL-1RA. IL-1RA deficient cells showed a reduced adherence and invasion by CFT073 compared to wild-type cells, suggesting that IL-1RA may oppose mechanisms that protects against bacterial colonization. A targeted protein analysis of inflammation-related proteins showed that the basal expression of 23 proteins and the UPEC-induced expression of 10 proteins were significantly altered in IL-1RA deficient bladder epithelial cells compared to Cas9 control cells. This suggests that IL-1RA has a broad effect on the inflammatory response in bladder epithelial cells.

Place, publisher, year, edition, pages
Academic Press, 2019
Keywords
IL-1 receptor antagonist, Inflammasome, NLRP3, Urinary tract infections, Uropathogenic Escherichia coli
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-75559 (URN)10.1016/j.cyto.2019.154772 (DOI)31299415 (PubMedID)
Available from: 2019-08-06 Created: 2019-08-06 Last updated: 2019-08-07Bibliographically approved
Engelsöy, U., Rangel, I. & Demirel, I. (2019). Impact of Proinflammatory Cytokines on the Virulence of Uropathogenic Escherichia coli. Frontiers in Microbiology, 10, Article ID 1051.
Open this publication in new window or tab >>Impact of Proinflammatory Cytokines on the Virulence of Uropathogenic Escherichia coli
2019 (English)In: Frontiers in Microbiology, ISSN 1664-302X, E-ISSN 1664-302X, Vol. 10, article id 1051Article in journal (Refereed) Published
Abstract [en]

The effect of a urinary tract infection on the host is a well-studied research field. However, how the host immune response affects uropathogenic Escherichia coli (CFT073) virulence is less studied. The aim of the present study was to investigate the impact of proinflammatory cytokine exposure on the virulence of uropathogenic Escherichia coli. We found that all tested proinflammatory cytokines (TNF-alpha, IL-1 beta, IL-6, IL-8 and IFN-gamma) induced an increased CFT073 growth. We also found that biofilm formation and hemolytic activity was reduced in the presence of all proinflammatory cytokines. However, a reduction in siderophore release was only observed in the presence of IL-1 beta, IL-6 and IL-8. Real time-qPCR showed that all proinflammatory cytokines except TNF-alpha significantly increased genes associated with the iron acquisition system in CFT073. We also found that the proinflammatory cytokines induced significant changes in type-1 fimbriae, P-fimbriae and gluconeogenetic genes. Furthermore, we also showed, using a Caenorhabditis elegans (C. elegans) killing assay that all cytokines decreased the survival of C. elegans worms significantly. Taken together, our findings show that proinflammatory cytokines have the ability to alter the virulence traits of UPEC.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2019
Keywords
uropathogenic Escherichia coli, proinflammatory cytokines, cross kingdom interaction, virulence, bacterial growth
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-74408 (URN)10.3389/fmicb.2019.01051 (DOI)000467422200001 ()
Note

Funding Agency:

Faculty of Medicine and Health at Örebro University

Available from: 2019-05-28 Created: 2019-05-28 Last updated: 2019-05-28Bibliographically approved
Asfaw Idosa, B., Kelly, A., Jacobsson, S., Demirel, I., Fredlund, H., Särndahl, E. & Persson, A. (2019). Neisseria meningitidis-Induced Caspase-1 Activation in Human Innate Immune Cells Is LOS-Dependent. Journal of Immunology Research, Article ID 6193186.
Open this publication in new window or tab >>Neisseria meningitidis-Induced Caspase-1 Activation in Human Innate Immune Cells Is LOS-Dependent
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2019 (English)In: Journal of Immunology Research, ISSN 2314-8861, E-ISSN 2314-7156, article id 6193186Article in journal (Refereed) Published
Abstract [en]

Meningococcal disease such as sepsis and meningitidis is hallmarked by an excessive inflammatory response. The causative agent, Neisseria meningitidis, expresses the endotoxin lipooligosaccharide (LOS) that is responsible for activation of immune cells and the release of proinflammatory cytokines. One of the most potent proinflammatory cytokines, interleukin-1 (IL-1), is activated following caspase-1 activity in the intracellular multiprotein complex called inflammasome. Inflammasomes are activated by a number of microbial factors as well as danger molecules by a two-step mechanismpriming and licensing of inflammasome activationbut there are no data available regarding a role for inflammasome activation in meningococcal disease. The aim of this study was to investigate if N. meningitidis activates the inflammasome and, if so, the role of bacterial LOS in this activation. Cells were subjected to N. meningitidis, both wild-type (FAM20) and its LOS-deficient mutant (lpxA), and priming as well as licensing of inflammasome activation was investigated. The wild-type LOS-expressing parental FAM20 serogroup C N. meningitidis (FAM20) strain significantly enhanced the caspase-1 activity in human neutrophils and monocytes, whereas lpxA was unable to induce caspase-1 activity as well as to induce IL-1 release. While the lpxA mutant induced a priming response, measured as increased expression of NLRP3 and IL1B, the LOS-expressing FAM20 further increased this priming. We conclude that although non-LOS components of N. meningitidis contribute to the priming of the inflammasome activity, LOS per se is to be considered as the central component of N. meningitidis virulence, responsible for both priming and licensing of inflammasome activation.

Place, publisher, year, edition, pages
Hindawi Publishing Corporation, 2019
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:oru:diva-74647 (URN)10.1155/2019/6193186 (DOI)000468500900001 ()
Available from: 2019-06-10 Created: 2019-06-10 Last updated: 2019-06-10Bibliographically approved
Demirel, I., Persson, A., Brauner, A., Särndahl, E., Kruse, R. & Persson, K. (2018). Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells. Frontiers in Cellular and Infection Microbiology, 8, Article ID 81.
Open this publication in new window or tab >>Activation of the NLRP3 Inflammasome Pathway by Uropathogenic Escherichia coli Is Virulence Factor-Dependent and Influences Colonization of Bladder Epithelial Cells
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2018 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 8, article id 81Article in journal (Refereed) Published
Abstract [en]

The NLRP3 inflammasome and IL-1 beta release have recently been suggested to be important for the progression of urinary tract infection (UTI). However, much is still unknown regarding the interaction of UPEC and the NLRP3 inflammasome. The purpose of this study was to elucidate what virulence factors uropathogenic Escherichia coil (UPEC) use to modulate NLRP3 inflammasome activation and subsequent IL-1 beta release and the role of NLRP3 for UPEC colonization of bladder epithelial cells. The bladder epithelial cell line 5637, CRISPR/Cas9 generated NLRP3, caspase-1 and mesotrypsin deficient cell lines and transformed primary bladder epithelial cells (HBLAK) were stimulated with UPEC isolates and the non-pathogenic MG1655 strain. We found that the UPEC strain CFT073, but not MG1655, induced an increased caspase-1 activity and IL-1 beta release from bladder epithelial cells. The increase was shown to be mediated by et-hemolysin activation of the NLRP3 inflammasome in an NE-kappa B-independent manner. The effect of-hemolysin on IL-1 beta release was biphasic, initially suppressive, later inductive. Furthermore, the phase-locked type-1-fimbrial ON variant of CFT073 inhibited caspase-1 activation and IL-1 beta release. In addition, the ability of CFT073 to adhere to and invade NLRP3 deficient cells was significantly reduced compare to wild-type cells. The reduced colonization of NLRP3-deficient cells was type-1 fimbriae dependent. In conclusion, we found that the NLRP3 inflammasome was important for type-1 fimbriae-dependent colonization of bladder epithelial cells and that both type-1 fimbriae and alpha-hemolysin can modulate the activity of the NLRP3 inflammasome.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
UPEC, NLRP3 inflammasome, IL-1 beta, alpha-hemolysin, type-1 fimbriae
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-66388 (URN)10.3389/fcimb.2018.00081 (DOI)000427407100001 ()2-s2.0-85043771169 (Scopus ID)
Note

Funding Agency:

Faculty of Medicine and Health at Örebro University 

Available from: 2018-04-09 Created: 2018-04-09 Last updated: 2018-08-20Bibliographically approved
Svensson, L., Poljakovic, M., Demirel, I., Sahlberg, C. & Persson, K. (2018). Host-Derived Nitric Oxide and Its Antibacterial Effects in the Urinary Tract. Advances in Microbial Physiology, 73, 1-62
Open this publication in new window or tab >>Host-Derived Nitric Oxide and Its Antibacterial Effects in the Urinary Tract
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2018 (English)In: Advances in Microbial Physiology, ISSN 0065-2911, E-ISSN 2162-5468, Vol. 73, p. 1-62Article, review/survey (Refereed) Published
Abstract [en]

Urinary tract infection (UTI) is one of the most common bacterial infections in humans, and the majority are caused by uropathogenic Escherichia coli (UPEC). The rising antibiotic resistance among UPEC and the frequent failure of antibiotics to effectively treat recurrent UTI and catheter-associated UTI motivate research on alternative ways of managing UTI. Abundant evidence indicates that the toxic radical nitric oxide (NO), formed by activation of the inducible nitric oxide synthase, plays an important role in host defence to bacterial infections, including UTI. The major source of NO production during UTI is from inflammatory cells, especially neutrophils, and from the uroepithelial cells that are known to orchestrate the innate immune response during UTI. NO and reactive nitrogen species have a wide range of antibacterial targets, including DNA, heme proteins, iron-sulfur clusters, and protein thiol groups. However, UPEC have acquired a variety of defence mechanisms for protection against NO, such as the NO-detoxifying enzyme flavohemoglobin and the NO-tolerant cytochrome bd-I respiratory oxidase. The cytotoxicity of NO-derived intermediates is nonspecific and may be detrimental to host cells, and a balanced NO production is crucial to maintain the tissue integrity of the urinary tract. In this review, we will give an overview of how NO production from host cells in the urinary tract is activated and regulated, the effect of NO on UPEC growth and colonization, and the ability of UPEC to protect themselves against NO. We also discuss the attempts that have been made to develop NO-based therapeutics for UTI treatment.

Place, publisher, year, edition, pages
Academic Press, 2018
Keywords
Antimicrobial factor, Flavohemoglobin, Inducible nitric oxide synthase, Nitric oxide, Nitrosative stress, Urinary bladder, Urinary tract infection, Uropathogenic E. coli
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-70674 (URN)10.1016/bs.ampbs.2018.05.001 (DOI)000452097400001 ()30262107 (PubMedID)2-s2.0-85048708739 (Scopus ID)
Available from: 2018-12-10 Created: 2018-12-10 Last updated: 2018-12-17Bibliographically approved
Lönn, J., Ljunggren, S., Klarström-Engström, K., Demirel, I., Bengtsson, T. & Karlsson, H. (2018). Lipoprotein modifications by gingipains of Porphyromonas gingivalis. Journal of Periodontal Research, 53(3), 403-413
Open this publication in new window or tab >>Lipoprotein modifications by gingipains of Porphyromonas gingivalis
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2018 (English)In: Journal of Periodontal Research, ISSN 0022-3484, E-ISSN 1600-0765, Vol. 53, no 3, p. 403-413Article in journal (Refereed) Published
Abstract [en]

BACKGROUND AND OBJECTIVE: Several studies have shown an association between periodontitis and cardiovascular disease (CVD). Atherosclerosis is the major cause of CVD, and a key event in the development of atherosclerosis is accumulation of lipoproteins within the arterial wall. Bacteria are the primary etiologic agents in periodontitis and Porphyromonas gingivalis is the major pathogen in the disease. Several studies support a role of modified low-density lipoprotein (LDL) in atherogenesis; however, the pathogenic stimuli that induce the changes and the mechanisms by which this occur are unknown. This study aims to identify alterations in plasma lipoproteins induced by the periodontopathic species of bacterium, P. gingivalis, in vitro.

MATERIAL AND METHODS: Plasma lipoproteins were isolated from whole blood treated with wild-type and gingipain-mutant (lacking either the Rgp- or Kgp gingipains) P. gingivalis by density/gradient-ultracentrifugation and were studied using 2-dimensional gel electrophoresis followed by matrix-assisted laser desorption/ionization mass spectrometry. Porphyromonas gingivalis-induced lipid peroxidation and antioxidant levels were measured by thiobarbituric acid-reactive substances and antioxidant assay kits, respectively, and lumiaggregometry was used for measurement of reactive oxygen species (ROS) and aggregation.

RESULTS: Porphyromonas gingivalis exerted substantial proteolytic effects on the lipoproteins. The Rgp gingipains were responsible for producing 2 apoE fragments, as well as 2 apoB-100 fragments, in LDL, and the Kgp gingipain produced an unidentified fragment in high-density lipoproteins. Porphyromonas gingivalis and its different gingipain variants induced ROS and consumed antioxidants. Both the Rgp and Kgp gingipains were involved in inducing lipid peroxidation.

CONCLUSIONS: Porphyromonas gingivalis has the potential to change the expression of lipoproteins in blood, which may represent a crucial link between periodontitis and CVD.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2018
Keywords
gingipains, lipoproteins, MALDI-TOF mass spectrometry, Porphyromonas gingivalis, two-dimensional gel electrophoresis
National Category
Pharmacology and Toxicology Dentistry
Identifiers
urn:nbn:se:oru:diva-64504 (URN)10.1111/jre.12527 (DOI)000432018000014 ()29341140 (PubMedID)2-s2.0-85040740217 (Scopus ID)
Funder
Knowledge FoundationStiftelsen Längmanska kulturfondenMagnus Bergvall Foundation
Available from: 2018-01-25 Created: 2018-01-25 Last updated: 2018-08-20Bibliographically approved
Jayaprakash, K., Demirel, I., Khalaf, H. & Bengtsson, T. (2018). Porphyromonas gingivalis-induced inflammatory responses in THP1 cells are altered by native and modified low-density lipoproteins in a strain-dependent manner. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 126(8), 667-677
Open this publication in new window or tab >>Porphyromonas gingivalis-induced inflammatory responses in THP1 cells are altered by native and modified low-density lipoproteins in a strain-dependent manner
2018 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 126, no 8, p. 667-677Article in journal (Refereed) Published
Abstract [en]

Strong epidemiological evidence supports an association between cardiovascular and periodontal disease and furthermore, the periodontopathogen Porphyromonas gingivalis has been identified in blood and from atheromatous plaques. Blood exposed to P.gingivalis shows an increased protein modification of low-density lipoprotein (LDL). In this study, we investigate the inflammatory responses of THP1 cells incubated with P.gingivalis and the effects of native or modified LDL on these responses. Reactive oxygen species (ROS) and IL-1 were observed in THP1 cells following infection with P.gingivalis ATCC33277 and W50. Caspase 1 activity was quantified in THP1 cells and correlated with IL-1 accumulation. Oxidized LDL (oxLDL) induced IL-1 release and CD36 expression on THP1 cells. Modified LDL co-stimulated with ATCC33277 exhibited regulatory effects on caspase 1 activity, IL-1 release and CD36 expression in THP1 cells, whereas W50 induced more modest responses in THP1 cells. In summary, we show that P.gingivalis is capable of inducing pro-inflammatory responses in THP1 cells, and native and modified LDL could alter these responses in a dose- and strain-dependent manner. Strain-dependent differences in THP1 cell responses could be due to the effect of P.gingivalis proteases, presence or absence of capsule and proteolytic transformation of native and modified LDL.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2018
Keywords
Periodontitis, caspase 1, CD36, inflammation, IL-1beta
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-68467 (URN)10.1111/apm.12860 (DOI)000440136000003 ()2-s2.0-85050727521 (Scopus ID)
Funder
Swedish Heart Lung FoundationKnowledge Foundation
Note

Funding Agency:

Foundation of Olle Engkvist

Available from: 2018-08-15 Created: 2018-08-15 Last updated: 2018-08-15Bibliographically approved
Månsson, E., Söderquist, B., Nilsdotter-Augustinsson, Å., Särndahl, E. & Demirel, I. (2018). Staphylococcus epidermidis from prosthetic joint infections induces lower IL-1 release from human neutrophils than isolates from normal flora. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 126(8), 678-684
Open this publication in new window or tab >>Staphylococcus epidermidis from prosthetic joint infections induces lower IL-1 release from human neutrophils than isolates from normal flora
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2018 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 126, no 8, p. 678-684Article in journal (Refereed) Published
Abstract [en]

The aim of this study was to test the hypothesis that Staphylococcus epidermidis isolated from prosthetic joint infections (PJIs) differs from S.epidermidis isolated from normal flora in terms of its capacity to induce activation of caspase-1 and release of IL-1 in human neutrophils. The amount of active caspase-1 was determined over 6h by detecting Ac-YVAD-AMC fluorescence in human neutrophils incubated with S.epidermidis isolates from PJIs (ST2) or normal flora. The amount of IL-1 was detected by ELISA in neutrophil supernatants after 6h of incubation. Mean IL-1 release was lower after incubation with S.epidermidis from PJIs compared to isolates from normal flora, but no statistically significant difference was found in active caspase-1. Substantial inter-individual differences in both active caspase-1 and IL-1 were noted. These results suggest that evasion of innate immune response, measured as reduced capacity to induce release of IL-1 from human neutrophils, might be involved in the predominance of ST2 in S.epidermidis PJIs, but that other microbe-related factors are probably also important.

Place, publisher, year, edition, pages
Wiley-Blackwell Publishing Inc., 2018
Keywords
Staphylococcus epidermidis, prosthesis-related infections, pathology, host-pathogen interactions, immunology, caspase-1, interleukin-1beta
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:oru:diva-68468 (URN)10.1111/apm.12861 (DOI)000440136000004 ()2-s2.0-85050768159 (Scopus ID)
Available from: 2018-08-15 Created: 2018-08-15 Last updated: 2018-09-07Bibliographically approved
Bang, C. S., Demirel, I., Kruse, R. & Persson, K. (2017). Global gene expression profiling and antibiotic susceptibility after repeated exposure to the carbon monoxide-releasing molecule-2 (CORM-2) in multidrug-resistant ESBL-producing uropathogenic Escherichia coli. PLoS ONE, 12(6), Article ID e0178541.
Open this publication in new window or tab >>Global gene expression profiling and antibiotic susceptibility after repeated exposure to the carbon monoxide-releasing molecule-2 (CORM-2) in multidrug-resistant ESBL-producing uropathogenic Escherichia coli
2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 6, article id e0178541Article in journal (Refereed) Published
Abstract [en]

Treatment of urinary tract infections is today a challenge due to the increasing prevalence of multidrug-resistant ESBL-producing uropathogenic Escherichia coli (UPEC). There is an urgent need for new treatment strategies for multidrug-resistant UPEC and preferably with targets that have low potential for development of resistance. Carbon monoxide-releasing molecules (CORMs) are novel and potent antibacterial agents. The present study examines the transcriptomic targets of CORM-2 in a multidrug-resistant ESBL-producing UPEC isolate in response to a single exposure to CORM-2 and after repeated exposure to CORM-2. The bacterial viability and minimal inhibitory concentration (MIC) were also examined after repeated exposure to CORM-2. Microarray analysis revealed that a wide range of processes were affected by CORM-2, including a general trend of down-regulation in energy metabolism and biosynthesis pathways and up-regulation of the SOS response and DNA repair. Several genes involved in virulence (ibpB), antibiotic resistance (marAB, mdtABC) and biofilm formation (bhsA, yfgF) were up-regulated, while some genes involved in virulence (kpsC, fepCEG, entABE), antibiotic resistance (evgA) and biofilm formation (artIP) were down-regulated. Repeated exposure to CORM-2 did not alter the gene expression patterns, the growth inhibitory response to CORM-2 or the MIC values for CORM-2, cefotaxime, ciprofloxacin and trimethoprim. This study identifies several enriched gene ontologies, modified pathways and single genes that are targeted by CORM-2 in a multidrug-resistant UPEC isolate. Repeated exposure to CORM-2 did not change the gene expression patterns or fold changes and the susceptibility to CORM-2 remained after repeated exposure.

Place, publisher, year, edition, pages
Public Library of Science, 2017
National Category
Microbiology
Research subject
Biomedicine
Identifiers
urn:nbn:se:oru:diva-58779 (URN)10.1371/journal.pone.0178541 (DOI)000402880700036 ()28591134 (PubMedID)2-s2.0-85020463890 (Scopus ID)
Note

Funding Agencies:

Faculty of Medicine and Health at Örebro University  

Nyckelfonden at Örebro University Hospital 

Available from: 2017-07-26 Created: 2017-07-26 Last updated: 2017-11-29Bibliographically approved
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