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Urban, Constantin F.
Alternative names
Publications (10 of 51) Show all publications
Lopes, J. P., Stylianou, M., Backman, E., Holmberg, S., Ekoff, M., Nilsson, G. & Urban, C. F. (2019). Cryptococcus neoformans Induces MCP-1 Release and Delays the Death of Human Mast Cells. Frontiers in Cellular and Infection Microbiology, 9, Article ID 289.
Open this publication in new window or tab >>Cryptococcus neoformans Induces MCP-1 Release and Delays the Death of Human Mast Cells
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2019 (English)In: Frontiers in Cellular and Infection Microbiology, E-ISSN 2235-2988, Vol. 9, article id 289Article in journal (Refereed) Published
Abstract [en]

Cryptococcosis, caused by the basidiomycete Cryptococcus neoformans, is a life-threatening disease affecting approximately one million people per year worldwide. Infection can occur when C. neoformans cells are inhaled by immunocompromised people. In order to establish infection, the yeast must bypass recognition and clearance by immune cells guarding the tissue. Using in vitro infections, we characterized the role of mast cells (MCs) in cryptococcosis. We found that MCs recognize C. neoformans and release inflammatory mediators such as tryptase and cytokines. From the latter group MCs released mainly CCL-2/MCP-1, a strong chemoattractant for monocytic cells. We demonstrated that supernatants of infected MCs recruit monocytes but not neutrophils. During infection with C. neoformans, MCs have a limited ability to kill the yeast depending on the serotype. C. neoformans, in turn, modulates the lifespan of MCs both, by presence of its polysaccharide capsule and by secreting soluble modulators. Taken together, MCs might have important contributions to fungal clearance during early stages of cryptocococis where these cells regulate recruitment of monocytes to mucosal tissues.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2019
Keywords
innate immunity, Cryptococcus neoformans, mast cells, monocytes, monocyte chemoattractant protein 1/CCL-2, fungi
National Category
Immunology in the medical area Microbiology in the medical area
Identifiers
urn:nbn:se:umu:diva-162849 (URN)10.3389/fcimb.2019.00289 (DOI)000480550400001 ()31456952 (PubMedID)
Available from: 2019-09-06 Created: 2019-09-06 Last updated: 2019-09-06Bibliographically approved
Singel, K. L., Grzankowski, K. S., Khan, A. N., Grimm, M. J., D'Auria, A. C., Morrell, K., . . . Segal, B. H. (2019). Mitochondrial DNA in the tumour microenvironment activates neutrophils and is associated with worse outcomes in patients with advanced epithelial ovarian cancer. British Journal of Cancer, 120(2), 207-217
Open this publication in new window or tab >>Mitochondrial DNA in the tumour microenvironment activates neutrophils and is associated with worse outcomes in patients with advanced epithelial ovarian cancer
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2019 (English)In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 120, no 2, p. 207-217Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Advanced cancer causes necrosis and releases damage-associated molecular patterns (DAMPs). Mitochondrial DAMPs activate neutrophils, including generation of neutrophil extracellular traps (NETs), which are injurious, thrombogenic, and implicated in metastasis. We hypothesised that extracellular mitochondrial DNA (mtDNA) in ascites from patients with epithelial ovarian cancer (EOC) would correlate with worse outcomes.

METHODS: Banked ascites supernatants from patients with newly diagnosed advanced EOC were analysed for mtDNA, neutrophil elastase, and activation of healthy donor neutrophils and platelets. TCGA was mined for expression of SELP and ELANE.

RESULTS: The highest quartile of ascites mtDNA correlated with reduced progression-free survival (PFS) and a higher likelihood of disease progression within 12-months following primary surgery (n = 68, log-rank, p = 0.0178). NETs were detected in resected tumours. Ascites supernatants chemoattracted neutrophils, induced NETs, and activated platelets. Ascites exposure rendered neutrophils suppressive, based on abrogation of ex vivo stimulated T cell proliferation. Increased SELP mRNA expression correlated with worse overall survival (n = 302, Cox model, p = 0.02).

CONCLUSION: In this single-centre retrospective analysis, ascites mtDNA correlated with worse PFS in advanced EOC. Mitochondrial and other DAMPs in ascites may activate neutrophil and platelet responses that facilitate metastasis and obstruct anti-tumour immunity. These pathways are potential prognostic markers and therapeutic targets.

Place, publisher, year, edition, pages
Nature Publishing Group, 2019
National Category
Cell and Molecular Biology Cancer and Oncology
Research subject
Infectious Diseases; cellforskning; Immunology
Identifiers
urn:nbn:se:umu:diva-156192 (URN)10.1038/s41416-018-0339-8 (DOI)000456328200009 ()30518816 (PubMedID)
Funder
NIH (National Institute of Health), R01CA188900NIH (National Institute of Health), T32CA108456NIH (National Institute of Health), T32CA085183NIH (National Institute of Health), K01LM012100
Available from: 2019-02-07 Created: 2019-02-07 Last updated: 2019-02-26Bibliographically approved
Urban, C. F. & Nett, J. E. (2019). Neutrophil extracellular traps in fungal infection. Seminars in Cell and Developmental Biology, 89, 47-57
Open this publication in new window or tab >>Neutrophil extracellular traps in fungal infection
2019 (English)In: Seminars in Cell and Developmental Biology, ISSN 1084-9521, E-ISSN 1096-3634, Vol. 89, p. 47-57Article in journal (Refereed) Published
Abstract [en]

Fungal infections are a continuously increasing problem in modern health care. Understanding the complex biology of the emerging pathogens and unraveling the mechanisms of host defense may form the basis for the development of more efficient diagnostic and therapeutic tools. Neutrophils play a pivotal role in the defense against fungal pathogens. These phagocytic hunters migrate towards invading fungal microorganisms and eradicate them by phagocytosis, oxidative burst and release of neutrophil extracellular traps (NETs). In the last decade, the process of NET formation has received unparalleled attention, with numerous studies revealing the relevance of this neutrophil function for control of various mycoses. Here, we describe NET formation and summarize its role as part of the innate immune defense against fungal pathogens. We highlight factors influencing the formation of these structures and molecular mechanisms employed by fungi to impair the formation of NETs or subvert their antifungal effects.

Place, publisher, year, edition, pages
Elsevier, 2019
Keywords
Aspergillus, Candida, Immunology, Neutrophil, Neutrophil extracellular trap (NET)
National Category
Microbiology in the medical area
Research subject
Infectious Diseases; Immunology
Identifiers
urn:nbn:se:umu:diva-156197 (URN)10.1016/j.semcdb.2018.03.020 (DOI)000463473400006 ()29601861 (PubMedID)
Funder
Swedish Research Council, VR-MH 2014-02281The Kempe Foundations, SMK1453NIH (National Institute of Health), K08 AI108727
Available from: 2019-02-07 Created: 2019-02-07 Last updated: 2019-04-26Bibliographically approved
Hosseinzadeh, A., Stylianou, M., Lopes, J. P., Müller, D. C., Häggman, A., Holmberg, S., . . . Urban, C. F. (2019). Stable Redox-Cycling Nitroxide Tempol has Antifungal and Immune-modulatory Properties. Frontiers in Microbiology, 10, Article ID 1843.
Open this publication in new window or tab >>Stable Redox-Cycling Nitroxide Tempol has Antifungal and Immune-modulatory Properties
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2019 (English)In: Frontiers in Microbiology, ISSN 1664-302X, E-ISSN 1664-302X, Vol. 10, article id 1843Article in journal (Refereed) Published
Abstract [en]

Invasive mycoses remain underdiagnosed and difficult to treat. Hospitalized individuals with compromised immunity increase in number and constitute the main risk group for severe fungal infections. Current antifungal therapy is hampered by slow and insensitive diagnostics and frequent toxic side effects of standard antifungal drugs. Identification of new antifungal compounds with high efficacy and low toxicity is therefore urgently required. We investigated the antifungal activity of tempol, a cell-permeable nitroxide. To narrow down possible mode of action we used RNA-seq technology and metabolomics to probe for pathways specifically disrupted in the human fungal pathogen Candida albicans due to tempol administration. We found genes upregulated which are involved in iron homeostasis, mitochondrial stress, steroid synthesis, and amino acid metabolism. In an ex vivo whole blood infection, tempol treatment reduced C. albicans colony forming units and at the same time increased the release of pro-inflammatory cytokines, such as interleukin 8 (IL-8, monocyte chemoattractant protein-1, and macrophage migration inhibitory factor). In a systemic mouse model, tempol was partially protective with a significant reduction of fungal burden in the kidneys of infected animals during infection onset. The results obtained propose tempol as a promising new antifungal compound and open new opportunities for the future development of novel therapies.

Keywords
antifungal activity, redox active, immunomodulators, candidiasis, Candida albicans, Candida glabrata
National Category
Microbiology in the medical area
Research subject
Infectious Diseases
Identifiers
urn:nbn:se:umu:diva-151596 (URN)10.3389/fmicb.2019.01843 (DOI)000481763300001 ()31481939 (PubMedID)
Funder
Swedish Research Council, 2014-02281The Kempe Foundations, 1453
Note

Originally included in thesis in manuscript form 

Available from: 2018-09-07 Created: 2018-09-07 Last updated: 2019-10-11Bibliographically approved
Lopes, J. P. & Urban, C. F. (2019). Visualizing Hypoxia in a Murine Model of Candida albicans Infection Using in vivo Biofluorencence. BIO-PROTOCOL, 9(15), Article ID UNSP e3326.
Open this publication in new window or tab >>Visualizing Hypoxia in a Murine Model of Candida albicans Infection Using in vivo Biofluorencence
2019 (English)In: BIO-PROTOCOL, ISSN 2331-8325, Vol. 9, no 15, article id UNSP e3326Article in journal (Refereed) Published
Abstract [en]

Candida albicans is a leading human fungal pathogen that uses several metabolic adaptations to escape immune cells and causes systemic disease. Here, we describe a protocol for measuring one of these adaptations, the ability to thrive in hypoxic niches. Hypoxia was generated after successful subdermal infection with C. albicans in a murine infection model. Hypoxia was measured using a fluorescent dye for carbonic anhydrase 9, a host enzyme active under hypoxic conditions. Emitted fluorescence was subsequently quantified using an IVIS system. This protocol was optimized for the use in subdermal infection in mice but has the potential to be adapted to other models of fungal infection.

Place, publisher, year, edition, pages
BIO-PROTOCOL, 2019
Keywords
Candida albicans, Subdermal infection, Hypoxia, IVIS, Mycology
National Category
Medical Biotechnology
Identifiers
urn:nbn:se:umu:diva-162304 (URN)10.21769/BioProtoc.3326 (DOI)000478805900012 ()
Available from: 2019-09-06 Created: 2019-09-06 Last updated: 2019-09-06Bibliographically approved
Thunström Salzer, A., Niemiec, M. J., Hosseinzadeh, A., Stylianou, M., Åstrom, F., Röhm, M., . . . Urban, C. F. (2018). Assessment of Neutrophil Chemotaxis Upon G-CSF Treatment of Healthy Stem Cell Donors and in Allogeneic Transplant Recipients. Frontiers in Immunology, 9, Article ID 1968.
Open this publication in new window or tab >>Assessment of Neutrophil Chemotaxis Upon G-CSF Treatment of Healthy Stem Cell Donors and in Allogeneic Transplant Recipients
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2018 (English)In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 9, article id 1968Article in journal (Refereed) Published
Abstract [en]

Neutrophils are crucial for the human innate immunity and constitute the majority of leukocytes in circulation. Thus, blood neutrophil counts serve as a measure for the immune system's functionality. Hematological patients often have low neutrophil counts due to disease or chemotherapy. To increase neutrophil counts and thereby preventing infections in high-risk patients, recombinant G-CSF is widely used as adjunct therapy to stimulate the maturation of neutrophils. In addition, G-CSF is utilized to recruit stem cells (SCs) into the peripheral blood of SC donors. Still, the actual functionality of neutrophils resulting from G-CSF treatment remains insufficiently understood. We tested the ex vivo functionality of neutrophils isolated from blood of G-CSF-treated healthy SC donors. We quantified chemotaxis, oxidative burst, and phagocytosis before and after treatment and detected significantly reduced chemotactic activity upon G-CSF treatment. Similarly, in vitro treatment of previously untreated neutrophils with G-CSF led to reduced chemotactic activity. In addition, we revealed that this effect persists in the allogeneic SC recipients up to 4 weeks after neutrophil engraftment. Our data indicates that neutrophil quantity, as a sole measure of immunocompetence in high-risk patients should be considered cautiously as neutrophil functionality might be affected by the primary treatment.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
neutrophil, granulocyte colony stimulating factor (G-CSF), allogeneic transplant, chemotaxis, hematopoietic stern cell donor
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:umu:diva-152255 (URN)10.3389/fimmu.2018.01968 (DOI)000444324800001 ()30254629 (PubMedID)
Funder
Västerbotten County Council
Available from: 2018-10-03 Created: 2018-10-03 Last updated: 2018-10-03Bibliographically approved
Crawford, A. C., Lehtovirta-Morley, L. E., Alamir, O., Niemiec, M. J., Alawfi, B., Alsarraf, M., . . . Wilson, D. (2018). Biphasic zinc compartmentalisation in a human fungal pathogen. PLoS Pathogens, 14(5), Article ID e1007013.
Open this publication in new window or tab >>Biphasic zinc compartmentalisation in a human fungal pathogen
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2018 (English)In: PLoS Pathogens, ISSN 1553-7366, E-ISSN 1553-7374, Vol. 14, no 5, article id e1007013Article in journal (Refereed) Published
Abstract [en]

Nutritional immunity describes the host-driven manipulation of essential micronutrients, including iron, zinc and manganese. To withstand nutritional immunity and proliferate within their hosts, pathogenic microbes must express efficient micronutrient uptake and homeostatic systems. Here we have elucidated the pathway of cellular zinc assimilation in the major human fungal pathogen Candida albicans. Bioinformatics analysis identified nine putative zinc transporters: four cytoplasmic-import Zip proteins (Zrt1, Zrt2, Zrt3 and orf19.5428) and five cytoplasmic-export ZnT proteins (orf19.1536/Zrc1, orf19.3874, orf19.3769, orf19.3132 and orf19.52). Only Zrt1 and Zrt2 are predicted to localise to the plasma membrane and here we demonstrate that Zrt2 is essential for C. albicans zinc uptake and growth at acidic pH. In contrast, ZRT1 expression was found to be highly pH dependent and could support growth of the ZRT2-null strain at pH 7 and above. This regulatory paradigm is analogous to the distantly related pathogenic mould, Aspergillus fumigatus, suggesting that pH-adaptation of zinc transport may be conserved in fungi and we propose that environmental pH has shaped the evolution of zinc import systems in fungi. Deletion of C. albicans ZRT2 reduced kidney fungal burden in wild type, but not in mice lacking the zinc-chelating antimicrobial protein calprotectin. Inhibition of zrt2 Delta growth by neutrophil extracellular traps was calprotectin-dependent. This suggests that, within the kidney, C. albicans growth is determined by pathogen-Zrt2 and host-calprotectin. As well as serving as an essential micronutrient, zinc can also be highly toxic and we show that C. albicans deals with this potential threat by rapidly compartmentalising zinc within vesicular stores called zincosomes. In order to understand mechanistically how this process occurs, we created deletion mutants of all five ZnT-type transporters in C. albicans. Here we show that, unlike in Saccharomyces cerevisiae, C. albicans Zrc1 mediates zinc tolerance via zincosomal zinc compartmentalisation. This novel transporter was also essential for virulence and liver colonisation in vivo. In summary, we show that zinc homeostasis in a major human fungal pathogen is a multi-stage process initiated by Zrtl/Zrt2-cellular import, followed by Zrcl-dependent intracellular compartmentalisation.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2018
National Category
Microbiology
Identifiers
urn:nbn:se:umu:diva-150701 (URN)10.1371/journal.ppat.1007013 (DOI)000434026400017 ()29727465 (PubMedID)
Available from: 2018-09-05 Created: 2018-09-05 Last updated: 2019-02-07Bibliographically approved
Lopes, J. P., Stylianou, M., Backman, E., Holmberg, S., Jass, J., Claesson, R. & Urban, C. F. (2018). Evasion of Immune Surveillance in Low Oxygen Environments Enhances Candida albicans Virulence.. mBio, 9(6), Article ID e02120-18.
Open this publication in new window or tab >>Evasion of Immune Surveillance in Low Oxygen Environments Enhances Candida albicans Virulence.
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2018 (English)In: mBio, ISSN 2161-2129, E-ISSN 2150-7511, Vol. 9, no 6, article id e02120-18Article in journal (Refereed) Published
Abstract [en]

Microbial colonizers of humans have evolved to adapt to environmental cues and to sense nutrient availability. Oxygen is a constantly changing environmental parameter in different host tissues and in different types of infection. We describe how Candida albicans, an opportunistic fungal pathogen, can modulate the host response under hypoxia and anoxia. We found that high infiltration of polymorphonuclear leukocytes (PMNs) to the site of infection contributes to a low oxygen milieu in a murine subdermal abscess. A persistent hypoxic environment did not affect viability or metabolism of PMNs. Under oxygen deprivation, however, infection with C. albicans disturbed specific PMN responses. PMNs were not able to efficiently phagocytose, produce ROS, or release extracellular DNA traps. Failure to launch an adequate response was caused by C. albicans cell wall masking of β-glucan upon exposure to low oxygen levels which hindered PAMP sensing by Dectin-1 on the surfaces of PMNs. This in turn contributed to immune evasion and enhanced fungal survival. The cell wall masking effect is prolonged by the accumulation of lactate produced by PMNs under low oxygen conditions. Finally, adaptation to oxygen deprivation increased virulence of C. albicans which we demonstrated using a Caenorhabditis elegans infection model.IMPORTANCE Successful human colonizers have evolved mechanisms to bypass immune surveillance. Infiltration of PMNs to the site of infection led to the generation of a low oxygen niche. Exposure to low oxygen levels induced fungal cell wall masking, which in turn hindered pathogen sensing and antifungal responses by PMNs. The cell wall masking effect was prolonged by increasing lactate amounts produced by neutrophil metabolism under oxygen deprivation. In an invertebrate infection model, C. albicans was able to kill infected C. elegans nematodes within 2 days under low oxygen conditions, whereas the majority of uninfected controls and infected worms under normoxic conditions survived. These results suggest that C. albicans benefited from low oxygen niches to increase virulence. The interplay of C. albicans with innate immune cells under these conditions contributed to the overall outcome of infection. Adaption to low oxygen levels was in addition beneficial for C. albicans by reducing susceptibility to selected antifungal drugs. Hence, immunomodulation of host cells under low oxygen conditions could provide a valuable approach to improve current antifungal therapies.

Place, publisher, year, edition, pages
American Society for Microbiology, 2018
Keywords
Candida albicans, PMN, abscesses, anoxia, beta-glucan, fungal cell wall, fungal masking, hypoxia, immune evasion, mycology, neutrophil
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:umu:diva-153288 (URN)10.1128/mBio.02120-18 (DOI)000454730100052 ()30401781 (PubMedID)
Funder
Swedish Research Council, VR-M 2014-02281Swedish Research Council, 2017-01681The Kempe Foundations, SMK-1453Helge Ax:son Johnsons stiftelse Knowledge Foundation, 20140180
Available from: 2018-11-16 Created: 2018-11-16 Last updated: 2019-01-25Bibliographically approved
Ginley, B. G., Emmons, T., Lutnick, B., Urban, C. F., Segal, B. H. & Sarder, P. (2017). Computational detection and quantification of human and mouse neutrophil extracellular traps in flow cytometry and confocal microscopy. Scientific Reports, 7(1), Article ID 17755.
Open this publication in new window or tab >>Computational detection and quantification of human and mouse neutrophil extracellular traps in flow cytometry and confocal microscopy
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2017 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 7, no 1, article id 17755Article in journal (Refereed) Published
Abstract [en]

Neutrophil extracellular traps (NETs) are extracellular defense mechanisms used by neutrophils, where chromatin is expelled together with histones and granular/cytoplasmic proteins. They have become an immunology hotspot, implicated in infections, but also in a diverse array of diseases such as systemic lupus erythematosus, diabetes, and cancer. However, the precise assessment of in vivo relevance in different disease settings has been hampered by limited tools to quantify occurrence of extracellular traps in experimental models and human samples. To expedite progress towards improved quantitative tools, we have developed computational pipelines to identify extracellular traps from an in vitro human samples visualized using the ImageStream® platform (Millipore Sigma, Darmstadt, Germany), and confocal images of an in vivo mouse disease model of aspergillus fumigatus pneumonia. Our two in vitro methods, tested on n = 363/n =145 images respectively, achieved holdout sensitivity/specificity 0.98/0.93 and 1/0.92. Our unsupervised method for thin lung tissue sections in murine fungal pneumonia achieved sensitivity/specificity 0.99/0.98 in n = 14 images. Our supervised method for thin lung tissue classified NETs with sensitivity/specificity 0.86/0.90. We expect that our approach will be of value for researchers, and have application in infectious and inflammatory diseases.

Place, publisher, year, edition, pages
Nature Publishing Group, 2017
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-143398 (URN)10.1038/s41598-017-18099-y (DOI)000418359600005 ()29259241 (PubMedID)
Available from: 2017-12-21 Created: 2017-12-21 Last updated: 2018-06-09Bibliographically approved
Niemiec, M. J., Grumaz, C., Ermert, D., Desel, C., Shankar, M., Lopes, J. P., . . . Urban, C. F. (2017). Dual transcriptome of the immediate neutrophil and Candida albicans interplay. BMC Genomics, 18, Article ID 696.
Open this publication in new window or tab >>Dual transcriptome of the immediate neutrophil and Candida albicans interplay
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2017 (English)In: BMC Genomics, ISSN 1471-2164, E-ISSN 1471-2164, Vol. 18, article id 696Article in journal (Refereed) Published
Abstract [en]

Background: Neutrophils are traditionally considered transcriptionally inactive. Compared to other immune cells, little is known about their transcriptional profile during interaction with pathogens. Methods: We analyzed the meta-transcriptome of the neutrophil-Candida albicans interplay and the transcriptome of C. albicans challenged with neutrophil extracellular traps (NETs) by RNA-Seq, considering yeast and hypha individually in each approach. Results: The neutrophil response to C. albicans yeast and hyphae was dominated by a morphotype-independent core response. However, 11 % of all differentially expressed genes were regulated in a specific manner when neutrophils encountered the hyphal form of C. albicans. While involving genes for transcriptional regulators, receptors, and cytokines, the neutrophil core response lacked typical antimicrobial effectors genes. Genes of the NOD-like receptor pathway, including NLRP3, were enriched. Neutrophil-and NET-provoked responses in C. albicans differed. At the same time, the Candida transcriptome upon neutrophil encounter and upon NET challenge included genes from various metabolic processes and indicate a mutual role of the regulators Tup1p, Efg1p, Hap43p, and Cap1p. Upon challenge with neutrophils and NETs, the overall Candida response was partially morphotype-specific. Yet again, actual oppositional regulation in yeasts and hyphae was only detected for the arginine metabolism in neutrophil-infecting C. albicans. Conclusions: Taken together, our study provides a comprehensive and quantitative transcript profile of the neutrophil-C. albicans interaction. By considering the two major appearances of both, neutrophils and C. albicans, our study reveals yet undescribed insights into this medically relevant encounter. Hence, our findings will facilitate future research and potentially inspire novel therapy developments.

Keywords
Candida, Neutrophils, Dual transcriptome, Extracellular traps, NOD-like receptor pathway, Nutritional immunity, Morphotype
National Category
Microbiology in the medical area
Research subject
Clinical Bacteriology
Identifiers
urn:nbn:se:umu:diva-102836 (URN)10.1186/s12864-017-4097-4 (DOI)000409208200002 ()
Note

Originally published in manuscript form with title [RNA-Seq transcription profile of the neutrophil: Candida albicans in vitro interaction]

Errata BMC Genomics (2017) 18:696 DOI: 10.1186/s12864-017-4097-4

Available from: 2015-05-07 Created: 2015-05-07 Last updated: 2018-06-07Bibliographically approved
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