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  • 1. Dolowschiak, Tamas
    et al.
    Mueller, Anna Angelika
    Pisan, Lynn Joanna
    Feigelman, Rounak
    Felmy, Boas
    Sellin, Mikael Erik
    Namineni, Sukumar
    Nguyen, Bidong Dinh
    Wotzka, Sandra Yvonne
    Heikenwalder, Mathias
    von Mering, Christian
    Mueller, Christoph
    Hardt, Wolf-Dietrich
    IFN-γ Hinders Recovery from Mucosal Inflammation during Antibiotic Therapy for Salmonella Gut Infection.2016In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 20, no 2Article in journal (Refereed)
    Abstract [en]

    Salmonella Typhimurium (S.Tm) causes acute enteropathy resolving after 4-7 days. Strikingly, antibiotic therapy does not accelerate disease resolution. We screened for factors blocking remission using a S.Tm enterocolitis model. The antibiotic ciprofloxacin clears pathogen stool loads within 3-24 hr, while gut pathology resolves more slowly (ψ50: ∼48 hr, remission: 6-9 days). This delayed resolution is mediated by an interferon-γ (IFN-γ)-dependent response that is triggered during acute infection and continues throughout therapy. Specifically, IFN-γ production by mucosal T and NK cells retards disease resolution by maintaining signaling through the transcriptional regulator STAT1 and boosting expression of inflammatory mediators like IL-1β, TNF, and iNOS. Additionally, sustained IFN-γ fosters phagocyte accumulation and hampers antimicrobial defense mediated by IL-22 and the lectin REGIIIβ. These findings reveal a role for IFN-γ in delaying resolution of intestinal inflammation and may inform therapies for acute Salmonella enteropathy, chronic inflammatory bowel diseases, or disease resolution during antibiotic treatment.

  • 2.
    Herp, Simone
    et al.
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany.
    Brugiroux, Sandrine
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany;Univ Clermont Auvergne, Microbes Intestine Inflammat & Host Susceptibil, INRA 2018, UMR 1071 Inserm,USC, Clermont Ferrand, France.
    Garzetti, Debora
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany;German Ctr Infect Res DZIF, Partner Site LMU Munich, D-80336 Munich, Germany.
    Ring, Diana
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany;German Ctr Infect Res DZIF, Partner Site LMU Munich, D-80336 Munich, Germany.
    Jochum, Lara M.
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany.
    Beutler, Markus
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany.
    Eberl, Claudia
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany.
    Hussain, Saib
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany.
    Walter, Steffi
    Robert Koch Inst, Project Grp 5, D-38855 Wernigerode, Germany.
    Gerlach, Roman G.
    Robert Koch Inst, Project Grp 5, D-38855 Wernigerode, Germany.
    Ruscheweyh, Hans J.
    Univ Tubingen, Ctr Bioinformat, Tubingen, Germany;Swiss Fed Inst Technol, Inst Microbiol, Dept Biol, Zurich, Switzerland.
    Huson, Daniel
    Univ Tubingen, Ctr Bioinformat, Tubingen, Germany.
    Selling, Mikael E.
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Slack, Emma
    Swiss Fed Inst Technol, Dept Hlth Sci & Technol, Inst Food Nutr & Hlth, Zurich, Switzerland.
    Hanson, Buck
    Univ Vienna, Dept Microbiol & Ecosyst Sci, Res Network Chem Meets Microbiol, Althanstr 14, A-1090 Vienna, Austria.
    Loy, Alexander
    Univ Vienna, Dept Microbiol & Ecosyst Sci, Res Network Chem Meets Microbiol, Althanstr 14, A-1090 Vienna, Austria.
    Baines, John F.
    Max Planck Inst Evolutionary Biol, August Thienemann Str 2, D-24306 Plon, Germany.
    Bausch, Philipp
    Univ Copenhagen, Dept Biol, Lab Genom & Mol Biomed, Univ Pk 13, DK-2100 Copenhagen, Denmark.
    Basic, Marijana
    Hannover Med Sch, Inst Lab Anim Sci, D-30625 Hannover, Germany;Hannover Med Sch, Cent Anim Facil, D-30625 Hannover, Germany.
    Bleich, Andre
    Hannover Med Sch, Inst Lab Anim Sci, D-30625 Hannover, Germany;Hannover Med Sch, Cent Anim Facil, D-30625 Hannover, Germany.
    Berry, David
    Univ Vienna, Dept Microbiol & Ecosyst Sci, Res Network Chem Meets Microbiol, Althanstr 14, A-1090 Vienna, Austria.
    Stecher, Baerbel
    Ludwig Maximilians Univ Munchen, Max von Pettenkofer Inst, Pettenkoferstr 9a, D-80336 Munich, Germany;German Ctr Infect Res DZIF, Partner Site LMU Munich, D-80336 Munich, Germany.
    Mucispirillum schaedleri Antagonizes Salmonella Virulence to Protect Mice against Colitis2019In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 25, no 5, p. 681-694.e8Article in journal (Refereed)
    Abstract [en]

    The microbiota and the gastrointestinal mucus layer play a pivotal role in protection against non-typhoidal Salmonella enterica serovar Typhimurium (S. Tm) colitis. Here, we analyzed the course of Salmonella colitis in mice lacking a functional mucus layer in the gut. Unexpectedly, in contrast to mucus-proficient littermates, genetically deficient mice were protected against Salmonellainduced gut inflammation in the streptomycin colitis model. This correlated with microbiota alterations and enrichment of the bacterial phylum Deferribacteres. Using gnotobiotic mice associated with defined bacterial consortia, we causally linked Mucispirillum schaedleri, currently the sole known representative of Deferribacteres present in the mammalian microbiota, to host protection against S. Tm colitis. Inhibition by M. schaedleri involves interference with S. Tm invasion gene expression, partly by competing for anaerobic electron acceptors. In conclusion, this study establishes M. schaedleri, a core member of the murine gut microbiota, as a key antagonist of S. Tm virulence in the gut.

  • 3. Kirienko, Natalia V.
    et al.
    Kirienko, Daniel R.
    Larkins-Ford, Jonah
    Wählby, Carolina
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Ruvkun, Gary
    Ausubel, Frederick M.
    Pseudomonas aeruginosa Disrupts Caenorhabditis elegans Iron Homeostasis, Causing a Hypoxic Response and Death2013In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 13, no 4, p. 406-416Article in journal (Refereed)
    Abstract [en]

    The opportunistic pathogen Pseudomonas aeruginosa causes serious human infections, but effective treatments and the mechanisms mediating pathogenesis remain elusive. Caenorhabditis elegans shares innate immune pathways with humans, making it invaluable to investigate infection. To determine how P. aeruginosa disrupts host biology, we studied how P. aeruginosa kills C. elegans in a liquid-based pathogenesis model. We found that P. aeruginosa-mediated killing does not require quorum-sensing pathways or host colonization. A chemical genetic screen revealed that iron chelators alleviate P. aeruginosa-mediated killing. Consistent with a role for iron in P. aeruginosa pathogenesis, the bacterial siderophore pyoverdin was required for virulence and was sufficient to induce a hypoxic response and death in the absence of bacteria. Loss of the C. elegans hypoxia-inducing factor HIF-1, which regulates iron homeostasis, exacerbated P. aeruginosa pathogenesis, further linking hypoxia and killing. As pyoverdin is indispensable for virulence in mice, pyoverdin-mediated hypoxia is likely to be relevant in human pathogenesis.

  • 4.
    Lauber, Chris
    et al.
    Tech Univ Dresden, Inst Med Informat & Biometry, D-01307 Dresden, Germany..
    Seitz, Stefan
    Heidelberg Univ, Dept Infect Dis, Mol Virol, D-69120 Heidelberg, Germany..
    Mattei, Simone
    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany..
    Suh, Alexander
    Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Ecology and Genetics, Evolutionary Biology.
    Beck, Juergen
    Univ Hosp Freiburg, Dept Internal Med Mol Biol 2, D-79106 Freiburg, Germany..
    Herstein, Jennifer
    Univ Southern Calif, Keck Sch Med, Dept Psychiat & Behav Sci, Los Angeles, CA 90033 USA..
    Boerold, Jacob
    Heidelberg Univ, Dept Infect Dis, Mol Virol, D-69120 Heidelberg, Germany..
    Salzburger, Walter
    Univ Basel, Inst Zool, CH-4051 Basel, Switzerland..
    Kaderali, Lars
    Tech Univ Dresden, Inst Med Informat & Biometry, D-01307 Dresden, Germany.;Univ Med Greifswald, Inst Bioinformat, D-17487 Greifswald, Germany..
    Briggs, John A. G.
    European Mol Biol Lab, Struct & Computat Biol Unit, D-69117 Heidelberg, Germany..
    Bartenschlager, Ralf
    Heidelberg Univ, Dept Infect Dis, Mol Virol, D-69120 Heidelberg, Germany.;German Canc Res Ctr, Div Virus Associated Carcinogenesis, D-69120 Heidelberg, Germany..
    Deciphering the Origin and Evolution of Hepatitis B Viruses by Means of a Family of Non-enveloped Fish Viruses2017In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 22, no 3, p. 387-399,e1-e6Article in journal (Refereed)
    Abstract [en]

    Hepatitis B viruses (HBVs), which are enveloped viruses with reverse-transcribed DNA genomes, constitute the family Hepadnaviridae. An outstanding feature of HBVs is their streamlined genome organization with extensive gene overlap. Remarkably, the similar to 1,100 bp open reading frame (ORF) encoding the envelope proteins is fully nested within the ORF of the viral replicase P. Here, we report the discovery of a diversified family of fish viruses, designated nackednaviruses, which lack the envelope protein gene, but otherwise exhibit key characteristics of HBVs including genome replication via proteinprimed reverse-transcription and utilization of structurally related capsids. Phylogenetic reconstruction indicates that these two virus families separated more than 400 million years ago before the rise of tetrapods. We show that HBVs are of ancient origin, descending from non-enveloped progenitors in fishes. Their envelope protein gene emerged de novo, leading to a major transition in viral lifestyle, followed by co-evolution with their hosts over geologic eras.

  • 5.
    Sellin, Mikael E.
    et al.
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Müller, Anna A.
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Felmy, Boas
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Dolowschiak, Tamas
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Diard, Médéric
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Tardivel, Aubry
    Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland.
    Maslowski, Kendle M.
    Department of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland; Laboratory for Intestinal Ecosystem, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama 230-0045, Japan.
    Wolf-Dietrich, Hardt
    Institute of Microbiology, ETH Zürich, 8093 Zürich, Switzerland.
    Epithelium-intrinsic NAIP/NLRC4 inflammasome drives infected enterocyte expulsion to restrict Salmonella replication in the intestinal mucosa2014In: Cell Host and Microbe, ISSN 1931-3128, E-ISSN 1934-6069, Vol. 16, no 2, p. 237-248Article in journal (Refereed)
    Abstract [en]

    The gut mucosal epithelium separates the host from the microbiota, but enteropathogens such as Salmonella Typhimurium (S.Tm) can invade and breach this barrier. Defenses against such acute insults remain incompletely understood. Using a murine model of Salmonella enterocolitis, we analyzed mechanisms limiting pathogen loads in the epithelium during early infection. Although the epithelium-invading S.Tm replicate initially, this intraepithelial replicative niche is restricted by expulsion of infected enterocytes into the lumen. This mechanism is compromised if inflammasome components (NAIP1-6, NLRC4, caspase-1/-11) are deleted, or ablated specifically in the epithelium, resulting in ∼100-fold higher intraepithelial loads and accelerated lymph node colonization. Interestingly, the cytokines downstream of inflammasome activation, interleukin (IL)-1α/β and IL-18, appear dispensable for epithelial restriction of early infection. These data establish the role of an epithelium-intrinsic inflammasome, which drives expulsion of infected cells to restrict the pathogen's intraepithelial proliferation. This may represent a general defense mechanism against mucosal infections.

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