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  • 1.
    Bergonzini, Anna
    et al.
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Avila-Cariño, Javier
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR).
    Lopez Chiloeches, Maria
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Frisan, Teresa
    Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR).
    The challenge of establishing immunocompetent human intestinal 3D modelsManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    Expression of typhoid toxin in Salmonella Typhimurium causes DNA damage, activating the DNA damage response (DDR), in absence of an inflammatory response in the colonic mucosa of infected mice. The anti-inflammatory effect is tissue specific and is not observed in the liver, suggesting that the local immune microenvironment modulates the DDR outcome.

    To assess the role of the immune cells in the DDR outcome induced by the genotoxigenic Salmonella, we have initiated the development of an immunocompetent 3D colonic mucosal model based on a collagen matrix containing colonic fibroblasts and different subtypes of immune cells, overlayed with colonic epithelial cells.

    Embedding of peripheral blood mononuclear cells in the collagen matrix did not influenced either the tissue integrity or the activation of the DDR, observed exclusively upon infection with the genotoxigenic strain. However, embedding of T cells, monocytes, or non-polarized macrophages altered the pattern of the DDR and the toxin specific effect was lost. Presence of macrophages was further associated with alteration of the epithelial layer integrity. This effect was infection-dependent, but not toxin specific.

    Our data demonstrated that addition of immune cells to a 3D mucosal model altered the DDR induced by a genotoxigenic bacterium, highlighting the need to develop and optimize immunocompetent in vitro models.

  • 2.
    Lopez Chiloeches, Maria
    et al.
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Bergonzini, Anna
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
    Martin, Océane C. B.
    Biological and Medical Sciences Department, University Bordeaux, Centre National de la Recherche Scientifique (CNRS), Institut de Biochimie et Génétique Cellulaires (IBGC), Unité Mixte de Recherche (UMR) 5095, Bordeaux, France.
    Bergstein, Nicole
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Erttmann, Saskia F.
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet). Infection Oncology Unit, Institute of Clinical Molecular Biology, Christian-Albrechts University of Kiel, Kiel, Germany.
    Aung, Kyaw Min
    Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
    Gekara, Nelson O.
    Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden; Institute of Medical Microbiology and Hygiene, Medical Center, University of Freiburg, Faculty of Medicine, Freiburg, Germany.
    Avila Cariño, Javier
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Pateras, Ioannis S.
    Second Department of Pathology, “Attikon” University Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
    Frisan, Teresa
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Genotoxin-producing Salmonella enterica induces tissue-specific types of DNA damage and DNA damage response outcomes2023Ingår i: Frontiers in Immunology, E-ISSN 1664-3224, Vol. 14, artikel-id 1270449Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Introduction: Typhoid toxin-expressing Salmonella enterica causes DNA damage in the intestinal mucosa in vivo, activating the DNA damage response (DDR) in the absence of inflammation. To understand whether the tissue microenvironment constrains the infection outcome, we compared the immune response and DDR patterns in the colon and liver of mice infected with a genotoxigenic strain or its isogenic control strain.

    Methods: In situ spatial transcriptomic and immunofluorescence have been used to assess DNA damage makers, activation of the DDR, innate immunity markers in a multiparametric analysis.

    Result: The presence of the typhoid toxin protected from colonic bacteria-induced inflammation, despite nuclear localization of p53, enhanced co-expression of type-I interferons (IfnbI) and the inflammasome sensor Aim2, both classic features of DNA-break-induced DDR activation. These effects were not observed in the livers of either infected group. Instead, in this tissue, the inflammatory response and DDR were associated with high oxidative stress-induced DNA damage.

    Conclusions: Our work highlights the relevance of the tissue microenvironment in enabling the typhoid toxin to suppress the host inflammatory response in vivo.

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  • 3.
    Stratoulias, Vassilis
    et al.
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden; Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
    Ruiz, Rocío
    Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC, Universidad de Sevilla, Seville, Spain.
    Kanatani, Shigeaki
    Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
    Osman, Ahmed M.
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Keane, Lily
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
    Armengol, Jose A.
    Department of Physiology, Anatomy and Cellular Biology, University of Pablo de Olavide, Seville, Spain.
    Rodríguez-Moreno, Antonio
    Department of Physiology, Anatomy and Cellular Biology, University of Pablo de Olavide, Seville, Spain.
    Murgoci, Adriana-Natalia
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
    García-Domínguez, Irene
    Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC, Universidad de Sevilla, Seville, Spain.
    Alonso-Bellido, Isabel
    Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC, Universidad de Sevilla, Seville, Spain.
    González Ibáñez, Fernando
    Department of Molecular Medicine, Université Laval, and Axe Neurosciences, Centre de Recherche du CHU de Québec-Université Laval, QC, Laval, Canada; Division of Medical Sciences, University of Victoria, BC, Victoria, Canada.
    Picard, Katherine
    Department of Molecular Medicine, Université Laval, and Axe Neurosciences, Centre de Recherche du CHU de Québec-Université Laval, QC, Laval, Canada; Division of Medical Sciences, University of Victoria, BC, Victoria, Canada.
    Vázquez-Cabrera, Guillermo
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden; Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC, Universidad de Sevilla, Seville, Spain.
    Posada-Pérez, Mercedes
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden; Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC, Universidad de Sevilla, Seville, Spain.
    Vernoux, Nathalie
    Department of Molecular Medicine, Université Laval, and Axe Neurosciences, Centre de Recherche du CHU de Québec-Université Laval, QC, Laval, Canada.
    Tejera, Dario
    Department of Neurodegenerative Diseases and Gerontopsychiatry, University of Bonn, Bonn, Germany.
    Grabert, Kathleen
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
    Cheray, Mathilde
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
    González-Rodríguez, Patricia
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
    Pérez-Villegas, Eva M.
    Department of Physiology, Anatomy and Cellular Biology, University of Pablo de Olavide, Seville, Spain.
    Martínez-Gallego, Irene
    Department of Physiology, Anatomy and Cellular Biology, University of Pablo de Olavide, Seville, Spain.
    Lastra-Romero, Alejandro
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Brodin, David
    Bioinformatics and Expression Analysis Core Facility, Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden.
    Avila-Cariño, Javier
    Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Teknisk-naturvetenskapliga fakulteten, Institutionen för molekylärbiologi (Teknisk-naturvetenskaplig fakultet).
    Cao, Yang
    Clinical Epidemiology and Biostatistics, School of Medical Sciences, Örebro University, Örebro, Sweden; Unit of Integrative Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Airavaara, Mikko
    Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland; Faculty of Pharmacy, Drug Research Program, University of Helsinki, Helsinki, Finland.
    Uhlén, Per
    Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.
    Heneka, Michael T.
    Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Belvaux, Luxembourg; Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, MA, Worcester, United States.
    Tremblay, Marie-Ève
    Department of Molecular Medicine, Université Laval, and Axe Neurosciences, Centre de Recherche du CHU de Québec-Université Laval, QC, Laval, Canada; Division of Medical Sciences, University of Victoria, BC, Victoria, Canada.
    Blomgren, Klas
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden; Department of Paediatric Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Venero, Jose L.
    Instituto de Biomedicina de Sevilla, IBiS/Hospital Universitario Virgen del Rocío/CSIC, Universidad de Sevilla, Seville, Spain.
    Joseph, Bertrand
    Institute of Environmental Medicine, Toxicology Unit, Karolinska Institutet, Stockholm, Sweden.
    ARG1-expressing microglia show a distinct molecular signature and modulate postnatal development and function of the mouse brain2023Ingår i: Nature Neuroscience, ISSN 1097-6256, E-ISSN 1546-1726, Vol. 26, s. 1008-1020Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Molecular diversity of microglia, the resident immune cells in the CNS, is reported. Whether microglial subsets characterized by the expression of specific proteins constitute subtypes with distinct functions has not been fully elucidated. Here we describe a microglial subtype expressing the enzyme arginase-1 (ARG1; that is, ARG1+ microglia) that is found predominantly in the basal forebrain and ventral striatum during early postnatal mouse development. ARG1+ microglia are enriched in phagocytic inclusions and exhibit a distinct molecular signature, including upregulation of genes such as Apoe, Clec7a, Igf1, Lgals3 and Mgl2, compared to ARG1– microglia. Microglial-specific knockdown of Arg1 results in deficient cholinergic innervation and impaired dendritic spine maturation in the hippocampus where cholinergic neurons project, which in turn results in impaired long-term potentiation and cognitive behavioral deficiencies in female mice. Our results expand on microglia diversity and provide insights into microglia subtype-specific functions.

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