Mattias Svensson group

Using human organotypic models to study interactions between human stromal and phagocyte cells in infection and inflammation.

This includes (1) identifying traits underlying lung tissue pathology in response to acute bacterial infection and cancer, and (2) defining pathways that contribute to progression of disease in necrotizing skin infections, and (3) discovering pathways of persistent inflammation in the target tissues of inflammatory bowel disease (IBD) and periodontal disease (PD). We wish to increase the understanding of inflammatory responses to pathogens locally and how interactions between stromal cells and phagocyte cells contribute to disease manifestations. This knowledge can be translated into the design of novel immunotherapies and treatment strategies that can be used to manage bacterial invasion and persistence, as well as pathological inflammation in order to restore tissue integrity.

However, studying the many processes involved in infectious and inflammatory diseases, as well as the functional properties of human stromal cells and phagocyte cells in specific tissues are difficult. Our approach of developing and using three-dimensional (3D) tissue models, so called organotypic models that mimic real tissues, provides unique tools to study interactions between human stromal cells and phagocyte cells present in live tissue and often missed in monolayer-based cell cultures.

Utilizing our unique human in vitro models together with relevant clinical samples, we aim at defining important aspects of phagocyte cell (dendritic cells, macrophages, monocytes, and neutrophils) and stromal cell (fibroblasts, and endothelial cells) interactions in different human settings, involving infectious diseases and cancers in epithelial tissues, as well as the chronic inflammatory diseases IBD and PD. In addition, our models provide unique tools for the identification and evaluation of the efficacy of antibiotics, small molecule inhibitors and biological treatments on bacterial clearance and management of inflammation.

Keywords: Organotypic models, stromal cells, phagocyte cells, infection, inflammation


Mattias Svensson, Julius Juarez, Magdalini Lourda, Sofia Björnfot. Photo: Bosse Johansson

Group Leader

Mattias Svensson, MSc, PhD, Associate Professor

Expertise in preclinical research in the field of infectious diseases, inflammation, and immunology, as well as cell and tissue biology. Main responsibility to create a milieu where excellent scientific progress can be made and ensure that doctoral students receive a high quality doctoral education and post docs get good quality supervision to develop their scientific independence.
Phone: + 46 8-585 87296

Post docs

Magdalini Lourda, PhD.

Expertise in molecular and cell biology in the field of chronic inflammation and cancer. Main responsibility to explore functional properties of monocytes in chronic inflammatory diseases.

Nikolai Siemens, PhD.

Expertise in microbiology and group A streptococcal virulence properties. Main responsibility to explore pathways that contribute to the progression of disease in necrotizing skin infections.


Sofia Björnfot, DDS, PhD-student

Expertise in multicolor flow cytometry analyses and oral tissue pathology. Main responsibility to explore functional properties of monocytes and macrophages i PD and develop a 3D tissue model for studies on inflammatory reactions to the microbial flora in oral tissue.

Puran Chen, MD, PhD-student

Expertise in live-imaging fluorescence analysis and lung diseases. Main responsibilities to further develop the 3D lung tissue model to explore macrophage and dendritic cell migratory behaviour, and study the influence of infection and non-small cell lung cancers on phagocyte cell functions.

Egle Kvedaraite, MD, PhD-student

Expertise in confocal imaging analysis and gastrointestinal inflammation. Main responsibilities to develop tools for multicolour flourescence imaging analyses of gut tissue, and explore pathways of persistent inflammation in IBD, with focus on stromal cells and neutrophils.

Others affiliated to the group

Elisabeth Boström, DDS. PhD. Affiliated dentist and co-supervisor for Sofia Björnfot.
Oscar Hammarfjord, DDS, PhD. Affiliated dentist and co-supervisor for Sofia Björnfot.

Former members of the group

Julius Juarez, PhD, postdoctoral studies completed 2013.
Anh Thu Nguyen Hoang, M. SC. Pharm, PhD-studies completed 2013.


Traits underlying lung tissue pathology in response to acute bacterial infection and cancer 

Here, we seek to increase our understanding of processes that regulate phagocyte cell distribution, activation, and migration in lung tissue under homeostatic conditions and in response to various perturbations, including acute bacterial infection or cancer metastasis.

Pulmonary inflammation and disease may occur as a consequence of dysregulated cross-talk between the airway epithelium, stromal cells and innate phagocyte cells. Using our organotypic model of human lung with dendritic cells and macrophages in combination with live-imaging fluorescence microscopy, we will identify mechanisms regulating phagocyte cell migratory behaviour in response to necrotizing infection caused by pathogenic Staphylococcus aureus. In addition, we will use the lung organotypic model to explore interactions between phagocyte cells and non-small-cell lung cancers. 

National academic collaborations: Professor Anna Norrby-Teglund, PhD; Professor Rolf Lewensohn, MD, PhD; Professor Staffan Strömblad, PhD; Professor Thomas Ekström, PhD, all at Karolinska Institutet, Stockholm, Sweden

International academic collaborations: Gayathri Arakere, PhD, Indian Institute of Science, Bangalore, India; Francois Vandenesch, MD, PhD, University of Lyon, Lyon, France; Professor Steinar Skrede, MD, PhD, Haukeland universitetssjukehus, Bergen, Norway.

Industry: Per Åberg, PhD; Kinga Balog; Danen Cunoosamy, PhD, all at Astra Zenceca, Möldnal.

Financial support: Karolinska Institutet and Stockholm County Council.

Defining pathways that contribute to progression of disease in necrotizing skin infections

Currently, there are significant gaps in our understanding of spatial and temporal events that determine why tissue sometimes fails to maintain its integrity once homeostasis is disturbed. Pathogens represent the main source of homeostatic stress, and the arising inflammation engages complex networks of cells and molecules, involved in clearing of infection, as well as tissue repair. The engagement of such networks and pathways may not always be compatible with the ultimate goal, which is the preservation of self. Deregulation of inflammatory reactions may lead to considerable tissue pathology. Using our organotypic model of human skin we will focus on identifying cellular and molecular pathways that can be triggered by pathogenic Streptococcus pyogenes and that promote bacterial invasion, dissemination, persistence as well as skin tissue injury and thereby provide a deeper understanding on human tissue inflammation and integrity in necrotizing infections.

National academic collaboration: Professor Anna Norrby-Teglund, PhD, Karolinska Institutet; Matthias Mörgelin, PhD, Lund University, Lund, Sweden.  

International academic and industrial collaborations: All partners of INFECT (

Financial support: Swedish Research Council, Framework grant on Infection and Antibiotics; EU, FP7 HEALTH INFECT (

Discovering pathways of persistent inflammation in the target tissue of inflammatory bowel disease (IBD) and periodontal disease (PD)

In periodontal disease (PD) it is it is speculated that chronic inflammation occurs, as innate immune cells, including monocytes and macrophages, are hyper-reactive to microbial stimuli. By using an in house developed organotypic model of human oral tissue combined with relevant clinical samples from PD patients we will explore monocyte differentiation potential and macrophage functional properties in response to microbial stimuli in oral tissue. 

The persistence of inflammation within the target tissues of inflammatory bowel disease (IBD) is associated with poor outcome and the risk of development of malignancies. We speculate that dysregulated interactions between innate immune cells, particular neutrophils, and stromal cells contribute to pathological tissue inflammation seen in IBD. By developing advanced multicolour fluorescent imaging analysis of whole tissue biopsy sections from colon, we will on the one hand investigate how stromal cells affect neutrophils, and on the other hand how neutrophils affect stromal cells to perpetuate inflammation and contribute to IBD pathogenesis. 

Financial support: Swedish Revenue Fund for research in preventive odontology, Svenska Tandläkare-Sällskapet, Karolinska Institutet.

National academic collaborations: Anders Gustafsson, OD, PhD, Professor; Elisabeth Boström, DDS, PhD; Professor Jan-Inge Henter, MD, PhD, all at Karolinska Institutet, Stockholm, Sweden ; Maja Ideström, MD, PhD, Karolinska University Hospital, Stockholm, Sweden.

International academic collaborations: Ben Owens, PhD, Oxford University, Oxford UK: Ben Marsland, PhD, Université de Lausanne, Lausanne, Switzerland; Professor Todd Reinhart, PhD, University of Pittsburgh, Pittsburgh, US.

Selected publications

Tissue-infiltrating neutrophils represent the main source of IL-23 in the colon of patients with IBD.
Kvedaraite E, Lourda M, Ideström M, Chen P, Olsson-Åkefeldt S, Forkel M, et al
Gut 2016 Oct;65(10):1632-41

Pulmonary tuberculosis patients with a vitamin D deficiency demonstrate low local expression of the antimicrobial peptide LL-37 but enhanced FoxP3+ regulatory T cells and IgG-secreting cells.
Rahman S, Rehn A, Rahman J, Andersson J, Svensson M, Brighenti S
Clin. Immunol. 2015 Feb;156(2):85-97

Modeling Mycobacterium tuberculosis early granuloma formation in experimental human lung tissue.
Parasa V, Rahman M, Ngyuen Hoang A, Svensson M, Brighenti S, Lerm M
Dis Model Mech 2014 Feb;7(2):281-8

Progression of clinical tuberculosis is associated with a Th2 immune response signature in combination with elevated levels of SOCS3.
Ashenafi S, Aderaye G, Bekele A, Zewdie M, Aseffa G, Hoang A, et al
Clin. Immunol. 2014 Apr;151(2):84-99

Detection of IL-17A-producing peripheral blood monocytes in Langerhans cell histiocytosis patients.
Lourda M, Olsson-Åkefeldt S, Gavhed D, Björnfot S, Clausen N, Hjalmars U, et al
Clin. Immunol. 2014 Jul;153(1):112-22

Technical advance: live-imaging analysis of human dendritic cell migrating behavior under the influence of immune-stimulating reagents in an organotypic model of lung.
Nguyen Hoang A, Chen P, Björnfot S, Högstrand K, Lock J, Grandien A, et al
J. Leukoc. Biol. 2014 Sep;96(3):481-9

Levels of alpha-toxin correlate with distinct phenotypic response profiles of blood mononuclear cells and with agr background of community-associated Staphylococcus aureus isolates.
Mairpady Shambat S, Haggar A, Vandenesch F, Lina G, van Wamel W, Arakere G, et al
PLoS ONE 2014 ;9(8):e106107

BCG-specific IgG-secreting peripheral plasmablasts as a potential biomarker of active tuberculosis in HIV negative and HIV positive patients.
Ashenafi S, Aderaye G, Zewdie M, Raqib R, Bekele A, Magalhaes I, et al
Thorax 2013 Mar;68(3):269-76

Prime-boost vaccination with rBCG/rAd35 enhances CD8⁺ cytolytic T-cell responses in lesions from Mycobacterium tuberculosis-infected primates.
Rahman S, Magalhaes I, Rahman J, Ahmed R, Sizemore D, Scanga C, et al
Mol. Med. 2012 May;18():647-58

Dendritic cell functional properties in a three-dimensional tissue model of human lung mucosa.
Nguyen Hoang A, Chen P, Juarez J, Sachamitr P, Billing B, Bosnjak L, et al
Am. J. Physiol. Lung Cell Mol. Physiol. 2012 Jan;302(2):L226-37

Stromal cell-derived CXCL12 and CCL8 cooperate to support increased development of regulatory dendritic cells following Leishmania infection.
Nguyen Hoang A, Liu H, Juaréz J, Aziz N, Kaye P, Svensson M
J. Immunol. 2010 Aug;185(4):2360-71

Innate killing of Leishmania donovani by macrophages of the splenic marginal zone requires IRF-7.
Phillips R, Svensson M, Aziz N, Maroof A, Brown N, Beattie L, et al
PLoS Pathog. 2010 Mar;6(3):e1000813

Compartmentalization of immune responses in human tuberculosis: few CD8+ effector T cells but elevated levels of FoxP3+ regulatory t cells in the granulomatous lesions.
Rahman S, Gudetta B, Fink J, Granath A, Ashenafi S, Aseffa A, et al
Am. J. Pathol. 2009 Jun;174(6):2211-24

Cannabinoids affect dendritic cell (DC) potassium channel function and modulate DC T cell stimulatory capacity.
Wacnik P, Luhr K, Hill R, Ljunggren H, Kristensson K, Svensson M
J. Immunol. 2008 Sep;181(5):3057-66

Posttranscriptional regulation of II10 gene expression allows natural killer cells to express immunoregulatory function.
Maroof A, Beattie L, Zubairi S, Svensson M, Stager S, Kaye P
Immunity 2008 Aug;29(2):295-305

Co-transplantation of stromal cells interferes with the rejection of allogeneic islet grafts.
Jacobson S, Kumagai-Braesch M, Tibell A, Svensson M, Flodström-Tullberg M
Ann. N. Y. Acad. Sci. 2008 Dec;1150():213-6

Induction of dendritic cell migration upon Toxoplasma gondii infection potentiates parasite dissemination.
Lambert H, Hitziger N, Dellacasa I, Svensson M, Barragan A
Cell. Microbiol. 2006 Oct;8(10):1611-23

Stromal cell-derived CXCL12 and CCL8 cooperate to support increased development of regulatory dendritic cells following Leishmania infection.
Nguyen Hoang A, Liu H, Juaréz J, Aziz N, Kaye P, Svensson M
J. Immunol. 2010 Aug;185(4):2360-71

Stromal cells direct local differentiation of regulatory dendritic cells.
Svensson M, Maroof A, Ato M, Kaye P
Immunity 2004 Dec;21(6):805-16

Open positions

We always want to get in touch with talented potential co-workers. If you are interested in doing research within our group, as a degree project or as a researcher, please contact the group leader Mattias Svensson.

Infectious Disease Medicine