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Zlatkov, N. & Uhlin, B. E. (2019). Absence of Global Stress Regulation in Escherichia coli Promotes Pathoadaptation and Novel c-di-GMP-dependent Metabolic Capability. Scientific Reports, 9, Article ID 2600.
Open this publication in new window or tab >>Absence of Global Stress Regulation in Escherichia coli Promotes Pathoadaptation and Novel c-di-GMP-dependent Metabolic Capability
2019 (English)In: Scientific Reports, ISSN 2045-2322, Vol. 9, article id 2600Article in journal (Refereed) Published
Abstract [en]

athoadaptive mutations linked to c-di-GMP signalling were investigated in neonatal meningitis-causing Escherichia coli (NMEC). The results indicated that NMEC strains deficient in RpoS (the global stress regulator) maintained remarkably low levels of c-di-GMP, a major bacterial sessility-motility switch. Deletion of ycgG2, shown here to encode a YcgG allozyme with c-di-GMP phosphodiesterase activity, and the restoration of RpoS led to a decrease in S-fimbriae, robustly produced in artificial urine, hinting that the urinary tract could serve as a habitat for NMEC. We showed that NMEC were skilled in aerobic citrate utilization in the presence of glucose, a property that normally does not exist in E. coli. Our data suggest that this metabolic novelty is a property of extraintestinal pathogenic E. coli since we reconstituted this ability in E. coli UTI89 (a cystitis isolate) via deactivation rpoS; additionally, a set of pyelonephritis E. coli isolates were shown here to aerobically use citrate in the presence of glucose. We found that the main reason for this metabolic capability is RpoS inactivation leading to the production of the citrate transporter CitT, exploited by NMEC for ferric citrate uptake dependent on YcgG2 (an allozyme with c-di-GMP phosphodiesterase activity).

Place, publisher, year, edition, pages
Nature Publishing Group, 2019
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:umu:diva-155827 (URN)10.1038/s41598-019-39580-w (DOI)000459399400069 ()30796316 (PubMedID)
Note

Originally included in thesis in manuscript form.

Available from: 2019-01-29 Created: 2019-01-29 Last updated: 2019-05-22Bibliographically approved
Ahmad, I., Karah, N., Nadeem, A., Wai, S. N. & Uhlin, B. E. (2019). Analysis of colony phase variation switch in Acinetobacter baumannii clinical isolates. PLoS ONE, 14(1), Article ID e0210082.
Open this publication in new window or tab >>Analysis of colony phase variation switch in Acinetobacter baumannii clinical isolates
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2019 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 1, article id e0210082Article in journal (Refereed) Published
Abstract [en]

Reversible switching between opaque and translucent colony formation is a novel feature of Acinetobacter baumannii that has been associated with variations in the cell morphology, surface motility, biofilm formation, antibiotic resistance and virulence. Here, we assessed a number of phenotypic alterations related to colony switching in A. baumannii clinical isolates belonging to different multi-locus sequence types. Our findings demonstrated that these phenotypic alterations were mostly strain-specific. In general, the translucent subpopulations of A. baumannii produced more dense biofilms, were more piliated, and released larger amounts of outer membrane vesicles (OMVs). In addition, the translucent subpopulations caused reduced fertility of Caenorhabditis elegans. When assessed for effects on the immune response in RAW 264.7 macrophages, the OMVs isolated from opaque subpopulations of A. baumannii appeared to be more immunogenic than the OMVs from the translucent form. However, also the OMVs from the translucent subpopulations had the potential to evoke an immune response. Therefore, we suggest that OMVs may be considered for development of new immunotherapeutic treatments against A. baumannii infections.

Place, publisher, year, edition, pages
Public Library Science, 2019
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-155634 (URN)10.1371/journal.pone.0210082 (DOI)000454952800043 ()30608966 (PubMedID)
Funder
Swedish Research Council, 2015-03007Swedish Research Council, 2015-06824Swedish Research Council, 2016-06598Swedish Research Council, 349-2007-8673Swedish Research Council, 829-2006-7431The Kempe Foundations, JCK-1527The Kempe Foundations, JCK-1724
Available from: 2019-01-25 Created: 2019-01-25 Last updated: 2019-01-25Bibliographically approved
Abbara, A., Rawson, T. M., Karah, N., El-Amin, W., Hatcher, J., Tajaldin, B., . . . Sparrow, A. (2018). A summary and appraisal of existing evidence of antimicrobial resistance in the Syrian conflict. International Journal of Infectious Diseases, 75, 26-33
Open this publication in new window or tab >>A summary and appraisal of existing evidence of antimicrobial resistance in the Syrian conflict
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2018 (English)In: International Journal of Infectious Diseases, ISSN 1201-9712, E-ISSN 1878-3511, Vol. 75, p. 26-33Article, review/survey (Refereed) Published
Abstract [en]

Antimicrobial resistance (AMR) in populations experiencing war has yet to be addressed, despite the abundance of contemporary conflicts and the protracted nature of twenty-first century wars, in combination with growing global concern over conflict-associated bacterial pathogens. The example of the Syrian conflict is used to explore the feasibility of using existing global policies on AMR in conditions of extreme conflict. The available literature on AMR and prescribing behaviour in Syria before and since the onset of the conflict in March 2011 was identified. Overall, there is a paucity of rigorous data before and since the onset of conflict in Syria to contextualize the burden of AMR. However, post onset of the conflict, an increasing number of studies conducted in neighbouring countries and Europe have reported AMR in Syrian refugees. High rates of multidrug resistance, particularly Gram-negative organisms, have been noted amongst Syrian refugees when compared with local populations. Conflict impedes many of the safeguards against AMR, creates new drivers, and exacerbates existing ones. Given the apparently high rates of AMR in Syria, in neighbouring countries hosting refugees, and in European countries providing asylum, this requires the World Health Organization and other global health institutions to address the causes, costs, and future considerations of conflict-related AMR as an issue of global governance. (c) 2018 The Authors. Published by Elsevier Ltd on behalf of International Society for Infectious Diseases.

Place, publisher, year, edition, pages
Elsevier, 2018
Keywords
Syria, Antimicrobial resistance, Conflict, Refugees
National Category
Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-152890 (URN)10.1016/j.ijid.2018.06.010 (DOI)000446213000006 ()29936319 (PubMedID)
Available from: 2018-10-31 Created: 2018-10-31 Last updated: 2018-10-31Bibliographically approved
Abbara, A., Rawson, T. M., Karah, N., El-Amin, W., Hatcher, J., Tajaldin, B., . . . Sparrow, A. (2018). Antimicrobial resistance in the context of the Syrian conflict: Drivers before and after the onset of conflict and key recommendations. International Journal of Infectious Diseases, 73, 1-6
Open this publication in new window or tab >>Antimicrobial resistance in the context of the Syrian conflict: Drivers before and after the onset of conflict and key recommendations
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2018 (English)In: International Journal of Infectious Diseases, ISSN 1201-9712, E-ISSN 1878-3511, Vol. 73, p. 1-6Article, review/survey (Refereed) Published
Abstract [en]

Current evidence describing antimicrobial resistance (AMR) in the context of the Syrian conflict is of poor quality and sparse in nature. This paper explores and reports the major drivers of AMR that were present in Syria pre-conflict and those that have emerged since its onset in March 2011. Drivers that existed before the conflict included a lack of enforcement of existing legislation to regulate over-the-counter antibiotics and notification of communicable diseases. This contributed to a number of drivers of AMR after the onset of conflict, and these were also compounded by the exodus of trained staff, the increase in overcrowding and unsanitary conditions, the increase in injuries, and economic sanctions limiting the availability of required laboratory medical materials and equipment. Addressing AMR in this context requires pragmatic, multifaceted action at the local, regional, and international levels to detect and manage potentially high rates of multidrug-resistant infections. Priorities are (1) the development of a competent surveillance system for hospital-acquired infections, (2) antimicrobial stewardship, and (3) the creation of cost-effective and implementable infection control policies. However, it is only by addressing the conflict and immediate cessation of the targeting of health facilities that the rehabilitation of the health system, which is key to addressing AMR in this context, can progress. 

Place, publisher, year, edition, pages
Elsevier, 2018
Keywords
Antimicrobial resistance, Syria, Conflict, Surveillance, Refugees
National Category
Infectious Medicine
Identifiers
urn:nbn:se:umu:diva-150645 (URN)10.1016/j.ijid.2018.05.008 (DOI)000440348300001 ()29793039 (PubMedID)2-s2.0-85048323122 (Scopus ID)
Available from: 2018-08-29 Created: 2018-08-29 Last updated: 2018-08-29Bibliographically approved
Nakao, R., Myint, S. L., Wai, S. N. & Uhlin, B. E. (2018). Enhanced Biofilm Formation and Membrane Vesicle Release by Escherichia coli Expressing a Commonly Occurring Plasmid Gene, kil. Frontiers in Microbiology, 9, Article ID 2605.
Open this publication in new window or tab >>Enhanced Biofilm Formation and Membrane Vesicle Release by Escherichia coli Expressing a Commonly Occurring Plasmid Gene, kil
2018 (English)In: Frontiers in Microbiology, ISSN 1664-302X, E-ISSN 1664-302X, Vol. 9, article id 2605Article in journal (Refereed) Published
Abstract [en]

Escherichia coli is one of the most prevalent microorganisms forming biofilms on indwelling medical devices, as well as a representative model to study the biology and ecology of biofilms. Here, we report that a small plasmid gene, kil, enhances biofilm formation of E coli. The kil gene is widely conserved among naturally occurring colicinogenic plasmids such as ColE1 plasmid, and is also present in some plasmid derivatives used as cloning vectors. First, we found that overexpression of the kil gene product dramatically increased biofilm mass enriched with extracellular DNA in the outer membrane-compromised strain RN102, a deep rough LPS mutant E. coli K-12 derivative. We also found that the kil-enhanced biofilm formation was further promoted by addition of physiologically relevant concentrations of Mg2+, not only in the case of RN102, but also with the parental strain BW25113, which retains intact core-oligosaccharide LPS. Biofilm formation by kil-expressing BW25113 strain (BW25113 kil+) was significantly inhibited by protease but not DNase I. In addition, a large amount of proteinous materials were released from the BW25113 kil+ cells. These materials contained soluble cytoplasmic and periplasmic proteins, and insoluble membrane vesicles (MVs). The kil-induced MVs were composed of not only outer membrane/periplasmic proteins, but also inner membrane/cytoplasmic proteins, indicating that MVs from both of the outer and inner membranes could be released into the extracellular milieu. Subcellular fractionation analysis revealed that the Kil proteins translocated to both the outer and inner membranes in whole cells of BW25113 kil+. Furthermore, the BW25113 kil+ showed not only reduced viability in the stationary growth phase, but also increased susceptibility to killing by predator bacteria, Vibrio cholerae expressing the type VI secretion system, despite no obvious change in morphology and physiology of the bacterial membrane under regular culture conditions. Taken together, our findings suggest that there is risk of increasing biofilm formation and spreading of numerous MVs releasing various cellular components due to kil gene expression. From another point of view, our findings could also offer efficient MV production strategies using a conditional kil vector in biotechnological applications.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
Escherichia coli, bacterial biofilms, membrane vesicles, kil, ColE1 plasmids
National Category
Microbiology Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-153543 (URN)10.3389/fmicb.2018.02605 (DOI)000449415700001 ()
Funder
Swedish Research Council, 2015-03007Swedish Research Council, 2015-06824Swedish Research Council, 2014-4401Swedish Research Council, 2016-06598Swedish Research Council, 349-2007-8673Swedish Research CouncilThe Kempe Foundations
Available from: 2018-11-26 Created: 2018-11-26 Last updated: 2018-11-26Bibliographically approved
Dongre, M., Singh, B., Aung, K. M., Larsson, P., Miftakhova, R. R., Persson, K., . . . Wai, S. N. (2018). Flagella-mediated secretion of a novel Vibrio cholerae cytotoxin affecting both vertebrate and invertebrate hosts. Communications Biology, 1, Article ID 59.
Open this publication in new window or tab >>Flagella-mediated secretion of a novel Vibrio cholerae cytotoxin affecting both vertebrate and invertebrate hosts
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2018 (English)In: Communications Biology, ISSN 2399-3642, Vol. 1, article id 59Article in journal (Refereed) Published
Abstract [en]

Using Caenorhabditis elegans as an infection host model for Vibrio cholerae predator interactions, we discovered a bacterial cytotoxin, MakA, whose function as a virulence factor relies on secretion via the flagellum channel in a proton motive force-dependent manner. The MakA protein is expressed from the polycistronic makDCBA (motility-associated killing factor) operon. Bacteria expressing makDCBA induced dramatic changes in intestinal morphology leading to a defecation defect, starvation and death in C. elegans. The Mak proteins also promoted V. cholerae colonization of the zebrafish gut causing lethal infection. A structural model of purified MakA at 1.9 Å resolution indicated similarities to members of a superfamily of bacterial toxins with unknown biological roles. Our findings reveal an unrecognized role for V. cholerae flagella in cytotoxin export that may contribute both to environmental spread of the bacteria by promoting survival and proliferation in encounters with predators, and to pathophysiological effects during infections.

Place, publisher, year, edition, pages
Springer Nature Publishing AG, 2018
National Category
Microbiology in the medical area
Research subject
Infectious Diseases; Molecular Biology
Identifiers
urn:nbn:se:umu:diva-155563 (URN)10.1038/s42003-018-0065-z (DOI)000461126500059 ()30271941 (PubMedID)
Available from: 2019-01-22 Created: 2019-01-22 Last updated: 2019-04-04Bibliographically approved
Zhang, Z., Aung, K. M., Uhlin, B. E. & Wai, S. N. (2018). Reversible senescence of human colon cancer cells after blockage of mitosis/cytokinesis caused by the CNF1 cyclomodulin from Escherichia coli. Scientific Reports, 8, Article ID 17780.
Open this publication in new window or tab >>Reversible senescence of human colon cancer cells after blockage of mitosis/cytokinesis caused by the CNF1 cyclomodulin from Escherichia coli
2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 17780Article in journal (Refereed) Published
Abstract [en]

Cytotoxic necrotizing factor 1 (CNF1), a protein toxin produced by extraintestinal pathogenic Escherichia coli, activates the Rho-family small GTPases in eukaryotic cell, thereby perturbing multiple cellular functions. Increasing epidemiological evidence suggests a link between CNF1 and human inflammatory bowel disease and colorectal cancer. At the cellular level, CNF1 has been hypothesized to reprogram cell fate towards survival due to the role in perturbing cell cycle and apoptosis. However, it remains undetermined how cells survive from CNF1 intoxication. In this work, we show that CNF1 treatment blocks mitosis/cytokinesis, elicits endoreplication and polyploidisation in cultured human colon cancer cells, and drives them into reversible senescence, which provides a survival route for cells via depolyploidisation. Senescence in CNF1-treated cells is demonstrated with upregulation of several senescence markers including senescence-associated β-galactosidase activity, p53, p21 and p16, and concomitant inhibition of the retinoblastoma protein phosphorylation. Importantly, progeny derived from CNF1 treatment exhibit genomic instability exemplified by increased aneuploidy and become more resistant to CNF1, but not to 5-fluorouracil and oxaliplatin, the two agents commonly used in chemotherapeutic treatment for colorectal cancer. These observations display survival features of the cell after CNF1 treatment that may have implications for the potential role of CNF1 in carcinogenesis.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-154870 (URN)10.1038/s41598-018-36036-5 (DOI)000452893700003 ()30542142 (PubMedID)2-s2.0-85058540678 (Scopus ID)
Available from: 2019-01-04 Created: 2019-01-04 Last updated: 2019-01-04Bibliographically approved
Singh, B., Mortezaei, N., Savarino, S. J., Uhlin, B. E., Bullitt, E. & Andersson, M. (2017). Antibodies damage the resilience of fimbriae, causing them to be stiff and tangled. Journal of Bacteriology, 199(1), Article ID e00665-16.
Open this publication in new window or tab >>Antibodies damage the resilience of fimbriae, causing them to be stiff and tangled
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2017 (English)In: Journal of Bacteriology, ISSN 0021-9193, E-ISSN 1098-5530, Vol. 199, no 1, article id e00665-16Article in journal (Refereed) Published
Abstract [en]

As adhesion fimbriae are a major virulence factor for many pathogenic Gram-negative bacteria, they are also potential targets for antibodies. Fimbriae are commonly required for initiating the colonization that leads to disease, and their success as adhesion organelles lies in their ability to both initiate and sustain bacte- rial attachment to epithelial cells. The ability of fimbriae to unwind and rewind their helical filaments presumably reduces their detachment from tissue surfaces with the shear forces that accompany significant fluid flow. Therefore, the disruption of func- tional fimbriae by inhibiting this resilience should have high potential for use as a vaccine to prevent disease. In this study, we show that two characteristic biome- chanical features of fimbrial resilience, namely, the extension force and the exten- sion length, are significantly altered by the binding of antibodies to fimbriae. The fimbriae that were studied are normally expressed on enterotoxigenic Escherichia coli, which are a major cause of diarrheal disease. This alteration in biomechanical properties was observed with bivalent polyclonal antifimbrial antibodies that recog- nize major pilin subunits but not with the Fab fragments of these antibodies. Thus, we propose that the mechanism by which bound antibodies disrupt the uncoiling of natural fimbria under force is by clamping together layers of the helical filament, thereby increasing their stiffness and reducing their resilience during fluid flow. In addition, we propose that antibodies tangle fimbriae via bivalent binding, i.e., by binding to two individual fimbriae and linking them together. Use of antibodies to disrupt physical properties of fimbriae may be generally applicable to the large number of Gram-negative bacteria that rely on these surface-adhesion molecules as an essential virulence factor.

I M P O R T A N C E Our study shows that the resiliency of colonization factor antigen I (CFA/I) and coli surface antigen 2 (CS2) fimbriae, which are current targets for vac- cine development, can be compromised significantly in the presence of antifimbrial antibodies. It is unclear how the humoral immune system specifically interrupts in- fection after the attachment of enterotoxigenic Escherichia coli (ETEC) to the epithe- lial surface. Our study indicates that immunoglobulins, in addition to their well- documented role in adaptive immunity, can mechanically damage the resilience of fimbriae of surface-attached ETEC, thereby revealing a new mode of action. Our data suggest a mechanism whereby antibodies coat adherent and free-floating bacteria to impede fimbrial resilience. Further elucidation of this possible mechanism is likely to inform the development and refinement of preventive vaccines against ETEC diar- rhea. 

Keywords
pili, IgG, vaccine, CFA/I, CS2, optical tweezers
National Category
Biophysics Immunology Other Physics Topics
Identifiers
urn:nbn:se:umu:diva-119692 (URN)10.1128/JB.00665-16 (DOI)000391288200018 ()
Funder
Swedish Research Council, 621- 2013-5379Swedish Research Council, 2012-4638NIH (National Institute of Health), RR025434
Note

Originally published in manuscript form with title "Antibodies damage fimbrial resilience, making them stiff and tangled"

Available from: 2016-04-25 Created: 2016-04-25 Last updated: 2018-06-07Bibliographically approved
Karah, N., Jolley, K. A., Hall, R. M. & Uhlin, B. E. (2017). Database for the ampC alleles in Acinetobacter baumannii. PLoS ONE, 12(5), Article ID e0176695.
Open this publication in new window or tab >>Database for the ampC alleles in Acinetobacter baumannii
2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 5, article id e0176695Article in journal (Refereed) Published
Abstract [en]

Acinetobacter baumannii is a troublesome opportunistic pathogen with a high capacity for clonal dissemination. We announce the establishment of a database for the ampC locus in A. baumannii, in which novel ampC alleles are differentiated based on the occurrence of >= 1 nucleotide change, regardless of whether it is silent or missense. The database is openly accessible at the pubmlst platform for A. baumannii (http://pubmlst.org/abaumannii/). Forty-eight distinctive alleles of the ampC locus have so far been identified and deposited in the database. Isolates from clonal complex 1 (CC1), according to the Pasteur multilocus sequence typing scheme, had a variety of the ampC locus alleles, including alleles 1, 3, 4, 5, 6, 7, 8, 13, 14, 17, and 18. On the other hand, isolates from CC2 had the ampC alleles 2, 3, 19, 20, 21, 22, 23, 24, 26, 27, 28, and 46. Allele 3 was characteristic for sequence types ST3 or ST32. The ampC alleles 10, 16, and 25 were characteristic for CC10, ST16, and CC25, respectively. Our study points out that novel gene databases, in which alleles are numbered based on differences in their nucleotide identities, should replace traditional records that use amino acid substitutions to define new alleles.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2017
National Category
Genetics
Identifiers
urn:nbn:se:umu:diva-136075 (URN)10.1371/journal.pone.0176695 (DOI)000400645000049 ()28459877 (PubMedID)
Available from: 2017-06-16 Created: 2017-06-16 Last updated: 2018-06-09Bibliographically approved
Dimova, L. G., Zlatkov, N., Verkade, H. J., Uhlin, B. E. & Tietge, U. J. F. (2017). High- cholesterol diet does not alter gut microbiota composition in mice. Nutrition & Metabolism, 14, Article ID 15.
Open this publication in new window or tab >>High- cholesterol diet does not alter gut microbiota composition in mice
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2017 (English)In: Nutrition & Metabolism, ISSN 1743-7075, E-ISSN 1743-7075, Vol. 14, article id 15Article in journal (Refereed) Published
Abstract [en]

Introduction: Western diet containing both saturated fat and cholesterol impairs cardio- metabolic health partly by modulating diversity and function of the microbiota. While diet containing only high fat has comparable effects, it is unclear how diets only enriched in cholesterol impact the microbiota. Therefore, we aimed to characterize the response of host and microbiota to a high cholesterol ( HC) diet in mice susceptible to cardio- metabolic disease. Methods: LDLR knockout mice received either 1.25% HC or no cholesterol containing control diet ( NC) for 12 weeks before characterizing host cholesterol metabolism and intestinal microbiota composition ( next generation sequencing). Results: HC diet substantially increased plasma ( 1.6- fold) and liver cholesterol levels ( 21- fold), biliary cholesterol secretion ( 4.5- fold) and fecal neutral sterol excretion ( 68- fold, each p < 0.001) but not fecal bile acid excretion. Interestingly, despite the profound changes in intestinal cholesterol homeostasis no differences in microbial composition between control and HC- fed mice were detected. In both groups the main phyla were Bacteroidetes ( 55%), Firmicutes ( 27%) and Verrucomicrobia ( 14%). Conclusion: Our results demonstrate that in mice HC diet alone does not alter the microbiota composition despite inducing substantial adaptive changes in whole body cholesterol homeostasis. The impact of Western diet on intestinal microbiota thus appears to be mediated exclusively by its high fat content.

Place, publisher, year, edition, pages
BIOMED CENTRAL LTD, 2017
Keywords
Diet, Cholesterol, microbiota, Ldlr-knockout, Bile, Neutral sterols
National Category
Nutrition and Dietetics
Identifiers
urn:nbn:se:umu:diva-136088 (URN)10.1186/s12986-017-0170-x (DOI)000396910300001 ()28239402 (PubMedID)
Available from: 2017-06-14 Created: 2017-06-14 Last updated: 2019-01-29Bibliographically approved
Projects
Symposium on Bacterial Cell Biology and Pathogenesis [2008-07427_VR]; Umeå UniversityThe roles and mechanisms of bacterial nucleoid proteins in control of gene expression [2009-05720_VR]; Umeå UniversityBacteria-host interactions: Mechanisms for expression of virulence factors in enterobacteria [2010-03031_VR]; Umeå UniversityA National FESEM Resource for training and research using high resolution Field Emission Scanning-EM and Cryo-technology [2011-06274_VR]; Umeå UniversityRole and mechanisms of bacterial nucleoid proteins in control of gene expression [2012-04638_VR]; Umeå UniversityOperation grant to a national Field Emission Scanning-Electron Microscopy resource for training and research using high resolution scanning electron microscopyand cryo-technology [2013-02076_VR]; Umeå UniversityCombinatorials: Novel drugs and drug combinations against bacterial growth, survival and persistence; from high-­? throughput screening to mechanism of action [2015-06824_VR]; Umeå UniversityBacterial virulence mechanisms of the opportunistic pathogen Acinetobacter baumannii and the versatile pathogen Escherichia coli. [2015-03007_VR]; Umeå UniversityMIMS - The Swedish EMBL node for Molecular Medicine [2016-06598_VR]; Umeå University
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0002-2991-8072

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