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Sjöstedt, Anders
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Publications (10 of 99) Show all publications
Müller, D. C., Kauppi, A., Edin, A., Gylfe, Å., Sjöstedt, A. B. & Johansson, A. (2019). Phospholipid Levels in Blood during Community-Acquired Pneumonia. PLoS ONE, 14(5), Article ID e0216379.
Open this publication in new window or tab >>Phospholipid Levels in Blood during Community-Acquired Pneumonia
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2019 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 5, article id e0216379Article in journal (Refereed) Published
Abstract [en]

Phospholipids, major constituents of bilayer cell membranes, are present in large amounts in pulmonary surfactant and play key roles in cell signaling. Here, we aim at finding clinically useful disease markers in community-acquired pneumonia (CAP) using comprehensive phospholipid profiling in blood and modeling of changes between sampling time points. Serum samples from 33 patients hospitalized with CAP were collected at admission, three hours after the start of intravenous antibiotics, Day 1 (at 12–24 h), Day 2 (at 36–48 h), and several weeks after recovery. A profile of 75 phospholipid species including quantification of the bioactive lysophosphatidylcholines (LPCs) was determined using liquid chromatography coupled to time-of-flight mass spectrometry. To control for possible enzymatic degradation of LPCs, serum autotaxin levels were examined. Twenty-two of the 33 patients with a clinical diagnosis of CAP received a laboratory-verified CAP diagnosis by microbial culture or microbial DNA detection by qPCR. All major phospholipid species, especially the LPCs, were pronouncedly decreased in the acute stage of illness. Total and individual LPC concentrations increased shortly after the initiation of antibiotic treatment, concentrations were at their lowest 3h after the initiation, and increased after Day 1. The total LPC concentration increased by a change ratio of 1.6–1.7 between acute illness and Day 2, and by a ratio of 3.7 between acute illness and full disease resolution. Autotaxin levels were low in acute illness and showed little changes over time, contradicting a hypothesis of enzymatic degradation causing the low levels of LPCs. In this sample of patients with CAP, the results demonstrate that LPC concentration changes in serum of patients with CAP closely mirrored the early transition from acute illness to recovery after the initiation of antibiotics. LPCs should be further explored as potential disease stage biomarkers in CAP and for their potential physiological role during recovery.

Place, publisher, year, edition, pages
Public Library of Science, 2019
Keywords
Community-acquired pneumonia, phospholipids, infection, diagnosis, metabolomics
National Category
Infectious Medicine
Identifiers
urn:nbn:se:umu:diva-147058 (URN)10.1371/journal.pone.0216379 (DOI)000467148400025 ()31063483 (PubMedID)
Note

Originally included in thesis in manuscript form 

Available from: 2018-04-25 Created: 2018-04-25 Last updated: 2019-06-12Bibliographically approved
Rzhepishevska, O. I., Limanska, N., Galkin, M., Lacoma, A., Lundquist, M., Sokol, D., . . . Ramstedt, M. (2018). Characterization of clinically relevant model bacterial strains of Pseudomonas aeruginosa for anti-biofilm testing of materials. Acta Biomaterialia, 76, 99-107
Open this publication in new window or tab >>Characterization of clinically relevant model bacterial strains of Pseudomonas aeruginosa for anti-biofilm testing of materials
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2018 (English)In: Acta Biomaterialia, ISSN 1742-7061, E-ISSN 1878-7568, Vol. 76, p. 99-107Article in journal (Refereed) Published
Abstract [en]

There is a great interest in developing novel anti-biofilm materials in order to decrease medical device-associated bacterial infections causing morbidity and high healthcare costs. However, the testing of novel materials is often done using bacterial lab strains that may not exhibit the same phenotype as clinically relevant strains infecting medical devices. Furthermore, no consensus of strain selection exists in the field, making results very difficult to compare between studies. In this work, 19 clinical isolates of Pseudomonas aeruginosa originating from intubated patients in an intensive care unit have been characterized and compared to the lab reference strain PAO1 and a rmlC lipopolysaccharide mutant of PAO1. The adhesion and biofilm formation was monitored, as well as cell properties such as hydrophobicity, zeta potential and motility. Two groups of isolates were observed: one with high adhesion to polymer surfaces and one with low adhesion (the latter including PAO1). Furthermore, detailed biofilm assays in a flow system were performed using five characteristic isolates from the two groups. Confocal microscopy showed that the adhesion and biofilm formation of four of these five strains could be reduced dramatically on zwitterionic surface coatings. However, one isolate with pronounced swarming colonized and formed biofilm also on the antifouling surface. We demonstrate that the biofilm properties of clinical isolates can differ greatly from that of a standard lab strain and propose two clinical model strains for testing of materials designed for prevention of biofilm formation in the respiratory tract. The methodology used could beneficially be applied for screening of other collections of pathogens to identify suitable model strains for in vitro biofilm testing.

Statement of Significance: Medical-device associated infections present a great challenge in health care. Therefore, much research is undertaken to prevent bacterial colonization of new types of biomaterials. The work described here characterizes, tests and presents a number of clinically relevant bacterial model strains for assessing biofilm formation by Pseudomonas aeruginosa. Such model strains are of importance as they may provide better predictability of lab testing protocols with respect to how well materials would perform in an infection situation in a patient. Furthermore, this study uses the strains to test the performance of polymer surfaces designed to repel bacterial adhesion and it is shown that the biofilm formation for four out of the five tested bacterial strains was reduced.

Place, publisher, year, edition, pages
Elsevier, 2018
Keywords
Clinical isolates, Pseudomonas aeruginosa, Antifouling, Model strain, Surface chemistry
National Category
Other Chemistry Topics
Identifiers
urn:nbn:se:umu:diva-150151 (URN)10.1016/j.actbio.2018.06.019 (DOI)000442055600010 ()29902594 (PubMedID)2-s2.0-8504885706 (Scopus ID)
Funder
Stiftelsen Olle Engkvist Byggmästare, 2014/660
Available from: 2018-07-11 Created: 2018-07-11 Last updated: 2018-09-10Bibliographically approved
Alam, A., Golovliov, I., Javed, E. & Sjöstedt, A. (2018). ClpB mutants of Francisella tularensis subspecies holarctica and tularensis are defective for type VI secretion and intracellular replication. Scientific Reports, 8, Article ID 11324.
Open this publication in new window or tab >>ClpB mutants of Francisella tularensis subspecies holarctica and tularensis are defective for type VI secretion and intracellular replication
2018 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 11324Article in journal (Refereed) Published
Abstract [en]

Francisella tularensis, a highly infectious, intracellular bacterium possesses an atypical type VI secretion system (T6SS), which is essential for the virulence of the bacterium. Recent data suggest that the HSP100 family member, ClpB, is involved in T6SS disassembly in the subspecies Francisella novicida. Here, we investigated the role of ClpB for the function of the T6SS and for phenotypic characteristics of the human pathogenic subspecies holarctica and tularensis. The Delta clpB mutants of the human live vaccine strain, LVS, belonging to subspecies holarctica, and the highly virulent SCHU S4 strain, belonging to subspecies tularensis, both showed extreme susceptibility to heat shock and low pH, severely impaired type VI secretion (T6S), and significant, but impaired intracellular replication compared to the wild-type strains. Moreover, they showed essentially intact phagosomal escape. Infection of mice demonstrated that both Delta clpB mutants were highly attenuated, but the SCHU S4 mutant showed more effective replication than the LVS strain. Collectively, our data demonstrate that ClpB performs multiple functions in the F. tularensis subspecies holarctica and tularensis and its function is important for T6S, intracellular replication, and virulence.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-150672 (URN)10.1038/s41598-018-29745-4 (DOI)000439965200017 ()30054549 (PubMedID)2-s2.0-85050803246 (Scopus ID)
Funder
Swedish Research Council, 2013-4581; 2013-8621
Available from: 2018-08-16 Created: 2018-08-16 Last updated: 2018-08-21Bibliographically approved
Eneslätt, K., Golovliov, I., Rydén, P. & Sjöstedt, A. (2018). Vaccine-mediated mechanisms controlling replication of Francisella tularensis in human peripheral blood mononuclear cells using a co-culture system. Frontiers in Cellular and Infection Microbiology, 8, Article ID 27.
Open this publication in new window or tab >>Vaccine-mediated mechanisms controlling replication of Francisella tularensis in human peripheral blood mononuclear cells using a co-culture system
2018 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 8, article id 27Article in journal (Refereed) Published
Abstract [en]

Cell-mediated immunity (CMI) is normally required for efficient protection against intracellular infections, however, identification of correlates is challenging and they are generally lacking. Francisella tularensis is a highly virulent, facultative intracellular bacterium and CMI is critically required for protection against the pathogen, but how this is effectuated in humans is poorly understood. To understand the protective mechanisms, we established an in vitro co-culture assay to identify how control of infection of F. tularensis is accomplished by human cells and hypothesized that the model will mimic in vivo immune mechanisms. Non-adherent peripheral blood mononuclear cells (PBMCs) were expanded with antigen and added to cultures with adherent PBMC infected with the human vaccine strain, LVS, or the highly virulent SCHU S4 strain. Intracellular numbers of F. tularensis was followed for 72 h and secreted and intracellular cytokines were analyzed. Addition of PBMC expanded from naïve individuals, i.e., those with no record of immunization to F. tularensis, generally resulted in little or no control of intracellular bacterial growth, whereas addition of PBMC from a majority of F. tularensis-immune individuals executed static and sometimes cidal effects on intracellular bacteria. Regardless of infecting strain, statistical differences between the two groups were significant, P < 0.05. Secretion of 11 cytokines was analyzed after 72 h of infection and significant differences with regard to secretion of IFN-γ, TNF, and MIP-1β was observed between immune and naïve individuals for LVS-infected cultures. Also, in LVS-infected cultures, CD4 T cells from vaccinees, but not CD8 T cells, showed significantly higher expression of IFN-γ, MIP-1β, TNF, and CD107a than cells from naïve individuals. The co-culture system appears to identify correlates of immunity that are relevant for the understanding of mechanisms of the protective host immunity to F. tularensis.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
F. tularensis, in vitro model, human immune response, IFN-gamma, TNF, MIP-1 beta, correlates of immunity
National Category
Microbiology in the medical area Immunology
Identifiers
urn:nbn:se:umu:diva-144645 (URN)10.3389/fcimb.2018.00027 (DOI)000424355900001 ()29468144 (PubMedID)
Available from: 2018-02-08 Created: 2018-02-08 Last updated: 2018-08-20Bibliographically approved
Bröms, J. E., Meyer, L. & Sjöstedt, A. (2017). A mutagenesis-based approach identifies amino acids in the N-terminal part of Francisella tularensis IglE that critically control type VI system-mediated secretion. Virulence, 8(6), 821-847
Open this publication in new window or tab >>A mutagenesis-based approach identifies amino acids in the N-terminal part of Francisella tularensis IglE that critically control type VI system-mediated secretion
2017 (English)In: Virulence, ISSN 2150-5594, E-ISSN 2150-5608, Vol. 8, no 6, p. 821-847Article in journal (Refereed) Published
Abstract [en]

The Gram-negative bacterium Francisella tularensis is the etiological agent of the zoonotic disease tularemia. Its life cycle is characterized by an ability to survive within phagocytic cells through phagosomal escape and replication in the cytosol, ultimately causing inflammasome activation and host cell death. Required for these processes is the Francisella Pathogenicity Island (FPI), which encodes a Type VI secretion system (T6SS) that is active during intracellular infection. In this study, we analyzed the role of the FPI-component IglE, a lipoprotein which we previously have shown to be secreted in a T6SS-dependent manner. We demonstrate that in F. tularensis LVS, IglE is an outer membrane protein. Upon infection of J774 cells, an Delta iglE mutant failed to escape from phagosomes, and subsequently, to multiply and cause cytopathogenicity. Moreover, Delta iglE was unable to activate the inflammasome, to inhibit LPS-stimulated secretion of TNF-alpha, and showed marked attenuation in the mouse model. In F. novicida, IglE was required for in vitro secretion of IglC and VgrG. A mutagenesis-based approach involving frameshift mutations and alanine substitution mutations within the first similar to 38 residues of IglE revealed that drastic changes in the sequence of the extreme N-terminus (residues 2-6) were well tolerated and, intriguingly, caused hyper-secretion of IglE during intracellular infection, while even subtle mutations further downstream lead to impaired protein function. Taken together, this study highlights the importance of IglE in F. tularensis pathogenicity, and the contribution of the N-terminus for all of the above mentioned processes.

Place, publisher, year, edition, pages
TAYLOR & FRANCIS INC, 2017
Keywords
Francisella pathogenicity island, Francisella tularensis, IglE, type VI secretion
National Category
Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-141228 (URN)10.1080/21505594.2016.1258507 (DOI)000412306100029 ()27830989 (PubMedID)
Available from: 2017-10-27 Created: 2017-10-27 Last updated: 2018-06-09Bibliographically approved
Desvars-Larrive, A., Liu, X., Hjertqvist, M., Sjöstedt, A., Johansson, A. & Ryden, P. (2017). High-risk regions and outbreak modelling of tularemia in humans. Epidemiology and Infection, 145(3), 482-490
Open this publication in new window or tab >>High-risk regions and outbreak modelling of tularemia in humans
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2017 (English)In: Epidemiology and Infection, ISSN 0950-2688, E-ISSN 1469-4409, Vol. 145, no 3, p. 482-490Article in journal (Refereed) Published
Abstract [en]

Sweden reports large and variable numbers of human tularemia cases, but the high-risk regions are anecdotally defined and factors explaining annual variations are poorly understood. Here, high-risk regions were identified by spatial cluster analysis on disease surveillance data for 1984-2012. Negative binomial regression with five previously validated predictors (including predicted mosquito abundance and predictors based on local weather data) was used to model the annual number of tularemia cases within the high-risk regions. Seven high-risk regions were identified with annual incidences of 3.8-44 cases/100 000 inhabitants, accounting for 56.4% of the tularemia cases but only 9.3% of Sweden's population. For all high-risk regions, most cases occurred between July and September. The regression models explained the annual variation of tularemia cases within most high-risk regions and discriminated between years with and without outbreaks. In conclusion, tularemia in Sweden is concentrated in a few high-risk regions and shows high annual and seasonal variations. We present reproducible methods for identifying tularemia high-risk regions and modelling tularemia cases within these regions. The results may help health authorities to target populations at risk and lay the foundation for developing an early warning system for outbreaks.

Place, publisher, year, edition, pages
CAMBRIDGE UNIV PRESS, 2017
Keywords
Epidemiology, modelling, spatial cluster analysis, tularemia
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-132814 (URN)10.1017/S0950268816002478 (DOI)000393759000010 ()27806741 (PubMedID)
Available from: 2017-05-04 Created: 2017-05-04 Last updated: 2018-06-09Bibliographically approved
Wallet, P., Benaoudia, S., Mosnier, A., Lagrange, B., Martin, A., Lindgren, H., . . . Henry, T. (2017). IFN-gamma extends the immune functions of Guanylate Binding Proteins to inflammasome-independent antibacterial activities during Francisella novicida infection. PLoS Pathogens, 13(10), Article ID e1006630.
Open this publication in new window or tab >>IFN-gamma extends the immune functions of Guanylate Binding Proteins to inflammasome-independent antibacterial activities during Francisella novicida infection
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2017 (English)In: PLoS Pathogens, ISSN 1553-7366, E-ISSN 1553-7374, Vol. 13, no 10, article id e1006630Article in journal (Refereed) Published
Abstract [en]

Guanylate binding proteins (GBPs) are interferon-inducible proteins involved in the cellintrinsic immunity against numerous intracellular pathogens. The molecular mechanisms underlying the potent antibacterial activity of GBPs are still unclear. GBPs have been functionally linked to the NLRP3, the AIM2 and the caspase-11 inflammasomes. Two opposing models are currently proposed to explain the GBPs-inflammasome link: i) GBPs would target intracellular bacteria or bacteria-containing vacuoles to increase cytosolic PAMPs release ii) GBPs would directly facilitate inflammasome complex assembly. Using Francisella novicida infection, we investigated the functional interactions between GBPs and the inflammasome. GBPs, induced in a type I IFN-dependent manner, are required for the F. novicida-mediated AIM2-inflammasome pathway. Here, we demonstrate that GBPs action is not restricted to the AIM2 inflammasome, but controls in a hierarchical manner the activation of different inflammasomes complexes and apoptotic caspases. IFN-gamma induces a quantitative switch in GBPs levels and redirects pyroptotic and apoptotic pathways under the control of GBPs. Furthermore, upon IFN-gamma priming, F. novicida-infected macrophages restrict cytosolic bacterial replication in a GBP-dependent and inflammasome-independent manner. Finally, in a mouse model of tularemia, we demonstrate that the inflammasome and the GBPs are two key immune pathways functioning largely independently to control F. novicida infection. Altogether, our results indicate that GBPs are the master effectors of IFN-gamma-mediated responses against F. novicida to control antibacterial immune responses in inflammasome-dependent and independent manners.

Place, publisher, year, edition, pages
Public Library Science, 2017
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:umu:diva-141986 (URN)10.1371/journal.ppat.1006630 (DOI)000414163300008 ()
Available from: 2017-12-06 Created: 2017-12-06 Last updated: 2018-06-09Bibliographically approved
Honn, M., Lindgren, H., Bharath, G. K. & Sjöstedt, A. (2017). Lack of OxyR and KatG Results in Extreme Susceptibility of Francisella tularensis LVS to Oxidative Stress and Marked Attenuation In vivo. Frontiers in Cellular and Infection Microbiology, 7, Article ID 14.
Open this publication in new window or tab >>Lack of OxyR and KatG Results in Extreme Susceptibility of Francisella tularensis LVS to Oxidative Stress and Marked Attenuation In vivo
2017 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 7, article id 14Article in journal (Refereed) Published
Abstract [en]

Francisella tularensis is an intracellular bacterium and as such is expected to encounter a continuous attack by reactive oxygen species (ROS) in its intracellular habitat and efficiently coping with oxidative stress is therefore essential for its survival. The oxidative stress response system of F tularensis is complex and includes multiple antioxidant enzymes and pathways, including the transcriptional regulator OxyR and the H2O2-decomposing enzyme catalase, encoded by katG. The latter is regulated by OxyR. A deletion of either of these genes, however, does not severely compromise the virulence of F tularensis and we hypothesized that if the bacterium would be deficient of both catalase and OxyR, then the oxidative defense and virulence of F tularensis would become severely hampered. To test this hypothesis, we generated a double deletion mutant, Delta oxyR/Delta katG, of F tularensis LVS and compared its phenotype to the parental LVS strain and the corresponding single deletion mutants. In accordance with the hypothesis, Delta oxyR/Delta katG was distinctly more susceptible than Delta oxyR and Delta katG to H2O2, ONOO-, and O-2(-), moreover, it hardly grew in mouse-derived BMDM or in mice, whereas Delta katG and Delta oxyR grew as well as F tularensis LVS in BMDM and exhibited only slight attenuation in mice. Altogether, the results demonstrate the importance of catalase and OxyR for a robust oxidative stress defense system and that they act cooperatively. The lack of both functions render F tularensis severely crippled to handle oxidative stress and also much attenuated for intracellular growth and virulence.

Keywords
Francisella tularensis, OxyR, KatG, oxidative stress, virulence
National Category
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy) Microbiology
Identifiers
urn:nbn:se:umu:diva-131634 (URN)10.3389/fcimb.2017.00014 (DOI)000392532700001 ()28174696 (PubMedID)
Available from: 2017-03-02 Created: 2017-03-02 Last updated: 2018-06-09Bibliographically approved
Golovliov, I., Lindgren, H., Eneslätt, K., Conlan, W., Mosnier, A., Henry, T. & Sjöstedt, A. (2016). An In Vitro Co-culture Mouse Model Demonstrates Efficient Vaccine-Mediated Control of Francisella tularensis SCHU S4 and Identifies Nitric Oxide as a Predictor of Efficacy. Frontiers in Cellular and Infection Microbiology, 6, Article ID 152.
Open this publication in new window or tab >>An In Vitro Co-culture Mouse Model Demonstrates Efficient Vaccine-Mediated Control of Francisella tularensis SCHU S4 and Identifies Nitric Oxide as a Predictor of Efficacy
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2016 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 6, article id 152Article in journal (Refereed) Published
Abstract [en]

Francisella tularensis is a highly virulent intracellular bacterium and cell-mediated immunity is critical for protection, but mechanisms of protection against highly virulent variants, such as the prototypic strain F. tularensis strain SCHU S4, are poorly understood. To this end, we established a co-culture system, based on splenocytes from naive, or immunized mice and in vitro infected bone marrow-derived macrophages that allowed assessment of mechanisms controlling infection with F. tularensis. We utilized the system to understand why the clpB gene deletion mutant, Delta clpB, of SCHU S4 shows superior efficacy as a vaccine in the mouse model as compared to the existing human vaccine, the live vaccine strain (LVS). Compared to naive splenocytes, Delta clpB-, or LVS-immune splenocytes conferred very significant control of a SCHU S4 infection and the Delta clpB-immune splenocytes were superior to the LVS-immune splenocytes. Cultures with the Delta clpB-immune splenocytes also contained higher levels of IFN-gamma, IL-17, and GM-CSF and nitric oxide, and T cells expressing combinations of IFN-gamma, TNF-alpha, and IL-17, than did cultures with LVS-immune splenocytes. There was strong inverse correlation between bacterial replication and levels of nitrite, an end product of nitric oxide, and essentially no control was observed when BMDM from iNOS(-/-) mice were infected. Collectively, the co-culture model identified a critical role of nitric oxide for protection against a highly virulent strain of F. tularensis.

Keywords
F. tularensis SCHU S4, in vitro co-culturemodel, mouse immune response, correlates of protection
National Category
Immunology Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-129814 (URN)10.3389/fcimb.2016.00152 (DOI)000388557800001 ()27933275 (PubMedID)
Available from: 2017-01-10 Created: 2017-01-09 Last updated: 2018-06-09Bibliographically approved
Lampe, E. O., Brenz, Y., Herrmann, L., Repnik, U., Griffiths, G., Zingmark, C., . . . Hagedorn, M. (2016). Dissection of Francisella-Host Cell Interactions in Dictyostelium discoideum. Applied and Environmental Microbiology, 82(5), 1586-1598
Open this publication in new window or tab >>Dissection of Francisella-Host Cell Interactions in Dictyostelium discoideum
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2016 (English)In: Applied and Environmental Microbiology, ISSN 0099-2240, E-ISSN 1098-5336, Vol. 82, no 5, p. 1586-1598Article in journal (Refereed) Published
Abstract [en]

Francisella bacteria cause severe disease in both vertebrates and invertebrates and include one of the most infectious human pathogens. Mammalian cell lines have mainly been used to study the mechanisms by which Francisella manipulates its host to replicate within a large variety of hosts and cell types, including macrophages. Here, we describe the establishment of a genetically and biochemically tractable infection model: the amoeba Dictyostelium discoideum combined with the fish pathogen Francisella noatunensis subsp. noatunensis. Phagocytosed F. noatunensis subsp. noatunensis interacts with the endosomal pathway and escapes further phagosomal maturation by translocating into the host cell cytosol. F. noatunensis subsp. noatunensis lacking IglC, a known virulence determinant required for Francisella intracellular replication, follows the normal phagosomal maturation and does not grow in Dictyostelium. The attenuation of the F. noatunensis subsp. noatunensis Delta iglC mutant was confirmed in a zebrafish embryo model, where growth of F. noatunensis subsp. noatunensis Delta iglC was restricted. In Dictyostelium, F. noatunensis subsp. noatunensis interacts with the autophagic machinery. The intracellular bacteria colocalize with autophagic markers, and when autophagy is impaired (Dictyostelium Delta atg1), F. noatunensis subsp. noatunensis accumulates within Dictyostelium cells. Altogether, the Dictyostelium-F. noatunensis subsp. noatunensis infection model recapitulates the course of infection described in other host systems. The genetic and biochemical tractability of the system allows new approaches to elucidate the dynamic interactions between pathogenic Francisella and its host organism.

Place, publisher, year, edition, pages
American Society for Microbiology, 2016
National Category
Microbiology in the medical area Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Identifiers
urn:nbn:se:umu:diva-119661 (URN)10.1128/AEM.02950-15 (DOI)000373338800023 ()
Available from: 2016-04-29 Created: 2016-04-25 Last updated: 2018-06-07Bibliographically approved
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