{"entity": "journal", "iuid": "48a282082d1e49ac913cf8766183014a", "timestamp": "2026-06-08T11:47:07.018Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/Cell%20Host%20Microbe.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/Cell%20Host%20Microbe"}}, "title": "Cell Host Microbe", "issn": "1934-6069", "issn-l": "1931-3128", "publications_count": 5, "publications": [{"entity": "publication", "iuid": "0effefb552b64f16b9d47b8e0bd4482f", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0effefb552b64f16b9d47b8e0bd4482f.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0effefb552b64f16b9d47b8e0bd4482f"}}, "title": "Characterization of a lipid-based jumbo phage compartment as a hub for early phage infection.", "authors": [{"family": "Mozumdar", "given": "Deepto", "initials": "D"}, {"family": "Fossati", "given": "Andrea", "initials": "A", "orcid": "0000-0001-5170-4903", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/658637b885384441943698722fad5944.json"}}, {"family": "Stevenson", "given": "Erica", "initials": "E"}, {"family": "Guan", "given": "Jingwen", "initials": "J"}, {"family": "Nieweglowska", "given": "Eliza", "initials": "E"}, {"family": "Rao", "given": "Sanjana", "initials": "S"}, {"family": "Agard", "given": "David", "initials": "D"}, {"family": "Swaney", "given": "Danielle L", "initials": "DL", "orcid": "0000-0001-6119-6084", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/56317207941d4aaf81ab4d55de5fcba4.json"}}, {"family": "Bondy-Denomy", "given": "Joseph", "initials": "J"}], "type": "journal article", "published": "2024-07-10", "journal": {"title": "Cell Host Microbe", "issn": "1934-6069", "issn-l": "1931-3128", "volume": "32", "issue": "7", "pages": "1050-1058.e7"}, "abstract": "Viral genomes are most vulnerable to cellular defenses at the start of the infection. A family of jumbo phages related to phage \u03a6KZ, which infects Pseudomonas aeruginosa, assembles a protein-based phage nucleus to protect replicating phage DNA, but how it is protected prior to phage nucleus assembly is unclear. We find that host proteins related to membrane and lipid biology interact with injected phage protein, clustering in an early phage infection (EPI) vesicle. The injected virion RNA polymerase (vRNAP) executes early gene expression until phage genome separation from the vRNAP and the EPI vesicle, moving into the nascent proteinaceous phage nucleus. Enzymes involved in DNA replication and CRISPR/restriction immune nucleases are excluded by the EPI vesicle. We propose that the EPI vesicle is rapidly constructed with injected phage proteins, phage DNA, host lipids, and host membrane proteins to enable genome protection, early transcription, localized translation, and to ensure faithful genome transfer to the proteinaceous nucleus.", "doi": "10.1016/j.chom.2024.05.016", "pmid": "38870941", "labels": {"Andrea Fossati": null, "DDLS Fellow": null}, "xrefs": [{"db": "mid", "key": "NIHMS2004244"}, {"db": "pmc", "key": "PMC11239273"}, {"db": "pii", "key": "S1931-3128(24)00188-4"}], "notes": [], "created": "2025-03-18T16:51:13.029Z", "modified": "2025-03-21T13:20:33.888Z"}, {"entity": "publication", "iuid": "a325f425be174b0e9ee28a6cf4c19dfe", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/a325f425be174b0e9ee28a6cf4c19dfe.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/a325f425be174b0e9ee28a6cf4c19dfe"}}, "title": "Mucispirillum schaedleri Antagonizes Salmonella Virulence to Protect Mice against Colitis.", "authors": [{"family": "Herp", "given": "Simone", "initials": "S"}, {"family": "Brugiroux", "given": "Sandrine", "initials": "S"}, {"family": "Garzetti", "given": "Debora", "initials": "D"}, {"family": "Ring", "given": "Diana", "initials": "D"}, {"family": "Jochum", "given": "Lara M", "initials": "LM"}, {"family": "Beutler", "given": "Markus", "initials": "M"}, {"family": "Eberl", "given": "Claudia", "initials": "C"}, {"family": "Hussain", "given": "Saib", "initials": "S"}, {"family": "Walter", "given": "Steffi", "initials": "S"}, {"family": "Gerlach", "given": "Roman G", "initials": "RG"}, {"family": "Ruscheweyh", "given": "Hans J", "initials": "HJ"}, {"family": "Huson", "given": "Daniel", "initials": "D"}, {"family": "Sellin", "given": "Mikael E", "initials": "ME"}, {"family": "Slack", "given": "Emma", "initials": "E"}, {"family": "Hanson", "given": "Buck", "initials": "B"}, {"family": "Loy", "given": "Alexander", "initials": "A"}, {"family": "Baines", "given": "John F", "initials": "JF"}, {"family": "Rausch", "given": "Philipp", "initials": "P"}, {"family": "Basic", "given": "Marijana", "initials": "M"}, {"family": "Bleich", "given": "Andr\u00e9", "initials": "A"}, {"family": "Berry", "given": "David", "initials": "D"}, {"family": "Stecher", "given": "B\u00e4rbel", "initials": "B"}], "type": "journal article", "published": "2019-05-08", "journal": {"title": "Cell Host Microbe", "issn": "1934-6069", "issn-l": "1931-3128", "volume": "25", "issue": "5", "pages": "681-694.e8"}, "abstract": "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 Salmonella-induced 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.", "doi": "10.1016/j.chom.2019.03.004", "pmid": "31006637", "labels": {"Mikael Sellin": null, "SciLifeLab Fellow": null}, "xrefs": [{"db": "pii", "key": "S1931-3128(19)30156-8"}], "notes": [], "created": "2020-10-05T15:12:17.993Z", "modified": "2022-11-04T11:32:16.455Z"}, {"entity": "publication", "iuid": "f673d79b1076414584994ef4c7a4b0b0", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f673d79b1076414584994ef4c7a4b0b0.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f673d79b1076414584994ef4c7a4b0b0"}}, "title": "Helicobacter pylori Adapts to Chronic Infection and Gastric Disease via pH-Responsive BabA-Mediated Adherence.", "authors": [{"family": "Bugaytsova", "given": "Jeanna A", "initials": "JA"}, {"family": "Bj\u00f6rnham", "given": "Oscar", "initials": "O"}, {"family": "Chernov", "given": "Yevgen A", "initials": "YA"}, {"family": "Gideonsson", "given": "P\u00e4r", "initials": "P"}, {"family": "Henriksson", "given": "Sara", "initials": "S"}, {"family": "Mendez", "given": "Melissa", "initials": "M"}, {"family": "Sj\u00f6str\u00f6m", "given": "Rolf", "initials": "R"}, {"family": "Mahdavi", "given": "Jafar", "initials": "J"}, {"family": "Shevtsova", "given": "Anna", "initials": "A"}, {"family": "Ilver", "given": "Dag", "initials": "D"}, {"family": "Moonens", "given": "Kristof", "initials": "K"}, {"family": "Quintana-Hayashi", "given": "Macarena P", "initials": "MP"}, {"family": "Moskalenko", "given": "Roman", "initials": "R"}, {"family": "Aisenbrey", "given": "Christopher", "initials": "C"}, {"family": "Bylund", "given": "G\u00f6ran", "initials": "G"}, {"family": "Schmidt", "given": "Alexej", "initials": "A"}, {"family": "\u00c5berg", "given": "Anna", "initials": "A"}, {"family": "Br\u00e4nnstr\u00f6m", "given": "Kristoffer", "initials": "K"}, {"family": "K\u00f6niger", "given": "Verena", "initials": "V"}, {"family": "Vikstr\u00f6m", "given": "Susanne", "initials": "S"}, {"family": "Rakhimova", "given": "Lena", "initials": "L"}, {"family": "Hofer", "given": "Anders", "initials": "A"}, {"family": "\u00d6gren", "given": "Johan", "initials": "J"}, {"family": "Liu", "given": "Hui", "initials": "H"}, {"family": "Goldman", "given": "Matthew D", "initials": "MD"}, {"family": "Whitmire", "given": "Jeannette M", "initials": "JM"}, {"family": "\u00c5d\u00e9n", "given": "J\u00f6rgen", "initials": "J"}, {"family": "Younson", "given": "Justine", "initials": "J"}, {"family": "Kelly", "given": "Charles G", "initials": "CG"}, {"family": "Gilman", "given": "Robert H", "initials": "RH"}, {"family": "Chowdhury", "given": "Abhijit", "initials": "A"}, {"family": "Mukhopadhyay", "given": "Asish K", "initials": "AK"}, {"family": "Nair", "given": "G Balakrish", "initials": "GB"}, {"family": "Papadakos", "given": "Konstantinos S", "initials": "KS"}, {"family": "Martinez-Gonzalez", "given": "Beatriz", "initials": "B"}, {"family": "Sgouras", "given": "Dionyssios N", "initials": "DN"}, {"family": "Engstrand", "given": "Lars", "initials": "L"}, {"family": "Unemo", "given": "Magnus", "initials": "M"}, {"family": "Danielsson", "given": "Dan", "initials": "D"}, {"family": "Suerbaum", "given": "Sebastian", "initials": "S"}, {"family": "Oscarson", "given": "Stefan", "initials": "S"}, {"family": "Morozova-Roche", "given": "Ludmilla A", "initials": "LA"}, {"family": "Olofsson", "given": "Anders", "initials": "A"}, {"family": "Gr\u00f6bner", "given": "Gerhard", "initials": "G"}, {"family": "Holgersson", "given": "Jan", "initials": "J"}, {"family": "Esberg", "given": "Anders", "initials": "A"}, {"family": "Str\u00f6mberg", "given": "Nicklas", "initials": "N"}, {"family": "Landstr\u00f6m", "given": "Mar\u00e9ne", "initials": "M"}, {"family": "Eldridge", "given": "Angela M", "initials": "AM"}, {"family": "Chromy", "given": "Brett A", "initials": "BA"}, {"family": "Hansen", "given": "Lori M", "initials": "LM"}, {"family": "Solnick", "given": "Jay V", "initials": "JV"}, {"family": "Lind\u00e9n", "given": "Sara K", "initials": "SK"}, {"family": "Haas", "given": "Rainer", "initials": "R"}, {"family": "Dubois", "given": "Andre", "initials": "A"}, {"family": "Merrell", "given": "D Scott", "initials": "DS"}, {"family": "Schedin", "given": "Staffan", "initials": "S"}, {"family": "Remaut", "given": "Han", "initials": "H"}, {"family": "Arnqvist", "given": "Anna", "initials": "A"}, {"family": "Berg", "given": "Douglas E", "initials": "DE"}, {"family": "Bor\u00e9n", "given": "Thomas", "initials": "T"}], "type": "journal article", "published": "2017-03-08", "journal": {"title": "Cell Host Microbe", "issn": "1934-6069", "volume": "21", "issue": "3", "pages": "376-389", "issn-l": "1931-3128"}, "abstract": "The BabA adhesin mediates high-affinity binding of Helicobacter pylori to the ABO blood group antigen-glycosylated gastric mucosa. Here we show that BabA is acid responsive-binding is reduced at low pH and restored by acid neutralization. Acid responsiveness differs among strains; often correlates with different intragastric regions and evolves during chronic infection and disease progression; and depends on pH sensor sequences in BabA and on pH reversible formation of high-affinity binding BabA multimers. We propose that BabA's extraordinary reversible acid responsiveness enables tight mucosal bacterial adherence while also allowing an effective escape from epithelial cells and mucus that are shed into the acidic bactericidal lumen and\u00a0that bio-selection and changes in BabA binding\u00a0properties through mutation and recombination with babA-related genes are selected by differences\u00a0among individuals and by changes in gastric acidity over time. These processes generate diverse H.\u00a0pylori subpopulations, in which BabA's adaptive evolution contributes to H.\u00a0pylori persistence and overt gastric disease.", "doi": "10.1016/j.chom.2017.02.013", "pmid": "28279347", "labels": {"Affiliated researcher": null}, "xrefs": [{"db": "pii", "key": "S1931-3128(17)30075-6"}, {"db": "pmc", "key": "PMC5392239"}, {"db": "mid", "key": "NIHMS855400"}], "notes": [], "created": "2018-12-05T10:22:52.648Z", "modified": "2018-12-05T10:22:52.667Z"}, {"entity": "publication", "iuid": "f40a92aeca1644c9bcd68adaa2f5e923", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f40a92aeca1644c9bcd68adaa2f5e923.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f40a92aeca1644c9bcd68adaa2f5e923"}}, "title": "IFN-\u03b3 Hinders Recovery from Mucosal Inflammation during Antibiotic Therapy for Salmonella Gut Infection.", "authors": [{"family": "Dolowschiak", "given": "Tamas", "initials": "T"}, {"family": "Mueller", "given": "Anna Angelika", "initials": "AA"}, {"family": "Pisan", "given": "Lynn Joanna", "initials": "LJ"}, {"family": "Feigelman", "given": "Rounak", "initials": "R"}, {"family": "Felmy", "given": "Boas", "initials": "B"}, {"family": "Sellin", "given": "Mikael Erik", "initials": "ME"}, {"family": "Namineni", "given": "Sukumar", "initials": "S"}, {"family": "Nguyen", "given": "Bidong Dinh", "initials": "BD"}, {"family": "Wotzka", "given": "Sandra Yvonne", "initials": "SY"}, {"family": "Heikenwalder", "given": "Mathias", "initials": "M"}, {"family": "von Mering", "given": "Christian", "initials": "C"}, {"family": "Mueller", "given": "Christoph", "initials": "C"}, {"family": "Hardt", "given": "Wolf-Dietrich", "initials": "WD"}], "type": "journal article", "published": "2016-08-10", "journal": {"title": "Cell Host Microbe", "issn": "1934-6069", "issn-l": "1931-3128", "volume": "20", "issue": "2", "pages": "238-249"}, "abstract": "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 (\u03c850: \u223c48 hr, remission: 6-9 days). This delayed resolution is mediated by an interferon-\u03b3 (IFN-\u03b3)-dependent response that is triggered during acute infection and continues throughout therapy. Specifically, IFN-\u03b3 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-1\u03b2, TNF, and iNOS. Additionally, sustained IFN-\u03b3 fosters phagocyte accumulation and hampers antimicrobial defense mediated by IL-22 and the lectin REGIII\u03b2. These findings reveal a role for IFN-\u03b3 in delaying resolution of intestinal inflammation and may inform therapies for acute Salmonella enteropathy, chronic inflammatory bowel diseases, or disease resolution during antibiotic treatment.", "doi": "10.1016/j.chom.2016.06.008", "pmid": "27453483", "labels": {"Mikael Sellin": null, "SciLifeLab Fellow": null}, "xrefs": [{"db": "pii", "key": "S1931-3128(16)30259-1"}], "notes": [], "created": "2018-12-03T14:40:52.369Z", "modified": "2022-11-04T11:32:19.310Z"}, {"entity": "publication", "iuid": "11964d40c69d4791a7f49bf3bd9e8bbc", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/11964d40c69d4791a7f49bf3bd9e8bbc.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/11964d40c69d4791a7f49bf3bd9e8bbc"}}, "title": "Pseudomonas aeruginosa disrupts Caenorhabditis elegans iron homeostasis, causing a hypoxic response and death.", "authors": [{"family": "Kirienko", "given": "Natalia V", "initials": "NV"}, {"family": "Kirienko", "given": "Daniel R", "initials": "DR"}, {"family": "Larkins-Ford", "given": "Jonah", "initials": "J"}, {"family": "W\u00e4hlby", "given": "Carolina", "initials": "C"}, {"family": "Ruvkun", "given": "Gary", "initials": "G"}, {"family": "Ausubel", "given": "Frederick M", "initials": "FM"}], "type": "journal article", "published": "2013-04-17", "journal": {"title": "Cell Host Microbe", "issn": "1934-6069", "volume": "13", "issue": "4", "pages": "406-416", "issn-l": "1931-3128"}, "abstract": "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.", "doi": "10.1016/j.chom.2013.03.003", "pmid": "23601103", "labels": {"Affiliated researcher": null}, "xrefs": [{"db": "pii", "key": "S1931-3128(13)00113-3"}, {"db": "pmc", "key": "PMC3641844"}, {"db": "mid", "key": "NIHMS462245"}], "notes": [], "created": "2018-12-05T08:56:00.700Z", "modified": "2018-12-05T08:56:00.730Z"}], "created": "2018-12-05T08:56:00.713Z", "modified": "2020-11-27T13:12:58.298Z"}