{"entity": "researcher", "timestamp": "2026-10-10T12:05:55.580Z", "family": "Hausmann", "given": "Annika", "initials": "A", "orcid": "0000-0001-8852-3444", "affiliations": ["Institute of Microbiology, Department of BiologyETH Zurich Zurich Switzerland"], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39"}}, "publications": [{"entity": "publication", "iuid": "cca33da747584cd1a658f60c209ca631", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/cca33da747584cd1a658f60c209ca631.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/cca33da747584cd1a658f60c209ca631"}}, "title": "Intraluminal neutrophils limit epithelium damage by reducing pathogen assault on intestinal epithelial cells during Salmonella gut infection.", "authors": [{"family": "G\u00fcl", "given": "Ersin", "initials": "E", "orcid": "0000-0003-2873-8034", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/dc90347a80ca48e28d2ab8293ce293e9.json"}}, {"family": "Enz", "given": "Ursina", "initials": "U"}, {"family": "Maurer", "given": "Luca", "initials": "L", "orcid": "0000-0002-9498-2775", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b81ff934767f4795b2244d13f9fb7ad5.json"}}, {"family": "Abi Younes", "given": "Andrew", "initials": "A"}, {"family": "Fattinger", "given": "Stefan A", "initials": "SA", "orcid": "0000-0003-4899-4414", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2a3891756a0e46b7be8494556da9254f.json"}}, {"family": "Nguyen", "given": "Bidong D", "initials": "BD"}, {"family": "Hausmann", "given": "Annika", "initials": "A", "orcid": "0000-0001-8852-3444", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39.json"}}, {"family": "Furter", "given": "Markus", "initials": "M"}, {"family": "Barthel", "given": "Manja", "initials": "M"}, {"family": "Sellin", "given": "Mikael E", "initials": "ME", "orcid": "0000-0002-8355-0803", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/559c18ec87d64318a0afc6267ea879e2.json"}}, {"family": "Hardt", "given": "Wolf-Dietrich", "initials": "WD", "orcid": "0000-0002-9892-6420", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1049556a73b84d258e26a84382fe5870.json"}}], "type": "journal article", "published": "2023-06-00", "journal": {"title": "PLoS Pathog", "issn": "1553-7374", "volume": "19", "issue": "6", "pages": "e1011235", "issn-l": "1553-7366"}, "abstract": "Recruitment of neutrophils into and across the gut mucosa is a cardinal feature of intestinal inflammation in response to enteric infections. Previous work using the model pathogen Salmonella enterica serovar Typhimurium (S.Tm) established that invasion of intestinal epithelial cells by S.Tm leads to recruitment of neutrophils into the gut lumen, where they can reduce pathogen loads transiently. Notably, a fraction of the pathogen population can survive this defense, re-grow to high density, and continue triggering enteropathy. However, the functions of intraluminal neutrophils in the defense against enteric pathogens and their effects on preventing or aggravating epithelial damage are still not fully understood. Here, we address this question via neutrophil depletion in different mouse models of Salmonella colitis, which differ in their degree of enteropathy. In an antibiotic pretreated mouse model, neutrophil depletion by an anti-Ly6G antibody exacerbated epithelial damage. This could be linked to compromised neutrophil-mediated elimination and reduced physical blocking of the gut-luminal S.Tm population, such that the pathogen density remained high near the epithelial surface throughout the infection. Control infections with a ssaV mutant and gentamicin-mediated elimination of gut-luminal pathogens further supported that neutrophils are protecting the luminal surface of the gut epithelium. Neutrophil depletion in germ-free and gnotobiotic mice hinted that the microbiota can modulate the infection kinetics and ameliorate epithelium-disruptive enteropathy even in the absence of neutrophil-protection. Together, our data indicate that the well-known protective effect of the microbiota is augmented by intraluminal neutrophils. After antibiotic-mediated microbiota disruption, neutrophils are central for maintaining epithelial barrier integrity during acute Salmonella-induced gut inflammation, by limiting the sustained pathogen assault on the epithelium in a critical window of the infection.", "doi": "10.1371/journal.ppat.1011235", "pmid": "37384776", "labels": {"SciLifeLab Fellow": "", "Mikael Sellin": ""}, "xrefs": [{"db": "pmc", "key": "PMC10337893"}, {"db": "pii", "key": "PPATHOGENS-D-23-00351"}], "notes": [], "created": "2023-12-01T13:09:47.879Z", "modified": "2026-09-23T10:54:17.714Z"}, {"entity": "publication", "iuid": "f661e59ccc0c4711b5934ab6937dff43", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f661e59ccc0c4711b5934ab6937dff43.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f661e59ccc0c4711b5934ab6937dff43"}}, "title": "Intercrypt sentinel macrophages tune antibacterial NF-\u03baB responses in gut epithelial cells via TNF.", "authors": [{"family": "Hausmann", "given": "Annika", "initials": "A", "orcid": "0000-0001-8852-3444", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39.json"}}, {"family": "Felmy", "given": "Boas", "initials": "B", "orcid": "0000-0002-9464-707X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6a2640ba7f7d431082ca196c9126664f.json"}}, {"family": "Kunz", "given": "Leo", "initials": "L", "orcid": "0000-0001-7332-3343", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/aa0495bb149440a3927920dbac7386a6.json"}}, {"family": "Kroon", "given": "Sanne", "initials": "S", "orcid": "0000-0002-5722-0763", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4ee4762c9bf94dd0a583281a4963cc35.json"}}, {"family": "Berthold", "given": "Doroth\u00e9e Lisa", "initials": "DL", "orcid": "0000-0002-9045-6348", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/53d7074e1b6947e28bf9a5cf47cf1b64.json"}}, {"family": "Ganz", "given": "Giverny", "initials": "G", "orcid": "0000-0003-1222-3781", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5a96e1234ca54a479945692585a6f196.json"}}, {"family": "Sandu", "given": "Ioana", "initials": "I", "orcid": "0000-0003-4696-0683", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a76cb953e62e486fab96331fc735232f.json"}}, {"family": "Nakamura", "given": "Toshihiro", "initials": "T", "orcid": "0000-0001-5051-4323", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7f99facb23c64d5a9080385014e90f8e.json"}}, {"family": "Zangger", "given": "Nathan S\u00e9bastien", "initials": "NS", "orcid": "0000-0003-1130-1899", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/71b7116da6bd4ecaa534c9dfa0f0a761.json"}}, {"family": "Zhang", "given": "Yang", "initials": "Y", "orcid": "0000-0002-1763-6908", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/7eb6794ef4be4579bb908fa4809a57b6.json"}}, {"family": "Dolowschiak", "given": "Tamas", "initials": "T", "orcid": "0000-0002-2031-9399", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6f1af24e9d6b4d92aa8dc0f72cfcf278.json"}}, {"family": "Fattinger", "given": "Stefan Alexander", "initials": "SA", "orcid": "0000-0003-4899-4414", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2a3891756a0e46b7be8494556da9254f.json"}}, {"family": "Furter", "given": "Markus", "initials": "M", "orcid": "0000-0003-4073-2268", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/51f09daa062347adb84d145a0128c608.json"}}, {"family": "M\u00fcller-Hauser", "given": "Anna Angelika", "initials": "AA", "orcid": "0000-0002-8031-2404", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/aa6eb65b570d4b6390871b05b6c824a6.json"}}, {"family": "Barthel", "given": "Manja", "initials": "M", "orcid": "0000-0001-6771-7661", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/adc1778ad09f4333abd2f45a29c113c1.json"}}, {"family": "Vlantis", "given": "Katerina", "initials": "K", "orcid": "0000-0002-7347-1589", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3739c46c24554582bd241f3cb16e1994.json"}}, {"family": "Wachsmuth", "given": "Laurens", "initials": "L", "orcid": "0000-0003-1701-9384", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4de7546893064de3af973373e7832d9e.json"}}, {"family": "Kisielow", "given": "Jan", "initials": "J", "orcid": "0000-0002-4482-5202", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/92846935bd80461886c261239645ff3f.json"}}, {"family": "Tortola", "given": "Luigi", "initials": "L", "orcid": "0000-0002-4335-412X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a7a1b0cfe81748839e5a02a9bd20745e.json"}}, {"family": "Heide", "given": "Danijela", "initials": "D", "orcid": "0000-0002-5670-7457", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6acd61a91f92460fa5e6e213d89eb201.json"}}, {"family": "Heikenw\u00e4lder", "given": "Mathias", "initials": "M", "orcid": "0000-0002-3135-2274", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5aeb664a4bb84c97862a3780a695a8e0.json"}}, {"family": "Oxenius", "given": "Annette", "initials": "A", "orcid": "0000-0002-2079-2354", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0a6c6eb9dca64e02b8ddbb63a1da33b5.json"}}, {"family": "Kopf", "given": "Manfred", "initials": "M", "orcid": "0000-0002-0628-7140", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0e378992386f4993a167c04aa529cf6f.json"}}, {"family": "Schroeder", "given": "Timm", "initials": "T", "orcid": "0000-0001-9320-0252", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/97c9fe7a450a4280837c4cd727cad137.json"}}, {"family": "Pasparakis", "given": "Manolis", "initials": "M", "orcid": "0000-0002-9870-0966", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a31f3861513f43e29c1ab07d465ddfcb.json"}}, {"family": "Sellin", "given": "Mikael Erik", "initials": "ME", "orcid": "0000-0002-8355-0803", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/559c18ec87d64318a0afc6267ea879e2.json"}}, {"family": "Hardt", "given": "Wolf-Dietrich", "initials": "WD", "orcid": "0000-0002-9892-6420", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1049556a73b84d258e26a84382fe5870.json"}}], "type": "journal article", "published": "2021-11-01", "journal": {"title": "J. Exp. Med.", "issn": "1540-9538", "volume": "218", "issue": "11", "issn-l": "0022-1007"}, "abstract": "Intestinal epithelial cell (IEC) NF-\u03baB signaling regulates the balance between mucosal homeostasis and inflammation. It is not fully understood which signals tune this balance and how bacterial exposure elicits the process. Pure LPS induces epithelial NF-\u03baB activation in vivo. However, we found that in mice, IECs do not respond directly to LPS. Instead, tissue-resident lamina propria intercrypt macrophages sense LPS via TLR4 and rapidly secrete TNF to elicit epithelial NF-\u03baB signaling in their immediate neighborhood. This response pattern is relevant also during oral enteropathogen infection. The macrophage-TNF-IEC axis avoids responses to luminal microbiota LPS but enables crypt- or tissue-scale epithelial NF-\u03baB responses in proportion to the microbial threat. Thereby, intercrypt macrophages fulfill important sentinel functions as first responders to Gram-negative microbes breaching the epithelial barrier. The tunability of this crypt response allows the induction of defense mechanisms at an appropriate scale according to the localization and intensity of microbial triggers.", "doi": "10.1084/jem.20210862", "pmid": "34529751", "labels": {"Mikael Sellin": "", "SciLifeLab Fellow": ""}, "xrefs": [{"db": "pmc", "key": "PMC8480669"}, {"db": "pii", "key": "212646"}], "notes": [], "created": "2021-12-05T09:46:45.613Z", "modified": "2026-09-23T10:35:05.173Z"}, {"entity": "publication", "iuid": "074bd7a0fee041f994069feb93fa3ecf", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/074bd7a0fee041f994069feb93fa3ecf.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/074bd7a0fee041f994069feb93fa3ecf"}}, "title": "Epithelium-autonomous NAIP/NLRC4 prevents TNF-driven inflammatory destruction of the gut epithelial barrier in Salmonella-infected mice.", "authors": [{"family": "Fattinger", "given": "Stefan A", "initials": "SA", "orcid": "0000-0003-4899-4414", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2a3891756a0e46b7be8494556da9254f.json"}}, {"family": "Geiser", "given": "Petra", "initials": "P", "orcid": "0000-0003-2785-4201", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0487e44d013c4faea6523a9f4b23cbe6.json"}}, {"family": "Samperio Ventayol", "given": "Pilar", "initials": "P", "orcid": "0000-0002-3726-7871", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e7647686922142a8b8bd8629142445fc.json"}}, {"family": "Di Martino", "given": "Maria Letizia", "initials": "ML", "orcid": "0000-0002-9491-4000", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ccaa06e9e2d441589299b7e33ee55034.json"}}, {"family": "Furter", "given": "Markus", "initials": "M", "orcid": "0000-0003-4073-2268", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/51f09daa062347adb84d145a0128c608.json"}}, {"family": "Felmy", "given": "Boas", "initials": "B"}, {"family": "Bakkeren", "given": "Erik", "initials": "E", "orcid": "0000-0001-7970-7890", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/374cea304e9d49129f59d95dfe72b72e.json"}}, {"family": "Hausmann", "given": "Annika", "initials": "A", "orcid": "0000-0001-8852-3444", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39.json"}}, {"family": "Barthel-Scherrer", "given": "Manja", "initials": "M"}, {"family": "G\u00fcl", "given": "Ersin", "initials": "E"}, {"family": "Hardt", "given": "Wolf-Dietrich", "initials": "WD", "orcid": "0000-0002-9892-6420", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1049556a73b84d258e26a84382fe5870.json"}}, {"family": "Sellin", "given": "Mikael E", "initials": "ME", "orcid": "0000-0002-8355-0803", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/559c18ec87d64318a0afc6267ea879e2.json"}}], "type": "journal article", "published": "2021-05-00", "journal": {"title": "Mucosal Immunol", "issn": "1935-3456", "volume": "14", "issue": "3", "pages": "615-629", "issn-l": "1933-0219"}, "abstract": "The gut epithelium is a critical protective barrier. Its NAIP/NLRC4 inflammasome senses infection by Gram-negative bacteria, including Salmonella Typhimurium (S.Tm) and promotes expulsion of infected enterocytes. During the first ~12-24 h, this reduces mucosal S.Tm loads at the price of moderate enteropathy. It remained unknown how this NAIP/NLRC4-dependent tradeoff would develop during subsequent infection stages. In NAIP/NLRC4-deficient mice, S.Tm elicited severe enteropathy within 72 h, characterized by elevated mucosal TNF (>20 pg/mg) production from bone marrow-derived cells, reduced regeneration, excessive enterocyte loss, and a collapse of the epithelial barrier. TNF-depleting antibodies prevented this destructive pathology. In hosts proficient for epithelial NAIP/NLRC4, a heterogeneous enterocyte death response with both apoptotic and pyroptotic features kept S.Tm loads persistently in check, thereby preventing this dire outcome altogether. Our results demonstrate that immediate and selective removal of infected enterocytes, by locally acting epithelium-autonomous NAIP/NLRC4, is required to avoid a TNF-driven inflammatory hyper-reaction that otherwise destroys the epithelial barrier.", "doi": "10.1038/s41385-021-00381-y", "pmid": "33731826", "labels": {"Mikael Sellin": "", "SciLifeLab Fellow": ""}, "xrefs": [{"db": "pmc", "key": "PMC8075861"}, {"db": "pii", "key": "S1933-0219(22)00163-5"}], "notes": [], "created": "2021-12-05T09:46:52.963Z", "modified": "2026-09-23T08:32:46.222Z"}, {"entity": "publication", "iuid": "f2e9187a61a443999aeb04e521d3967a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/f2e9187a61a443999aeb04e521d3967a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/f2e9187a61a443999aeb04e521d3967a"}}, "title": "Germ-free and microbiota-associated mice yield small intestinal epithelial organoids with equivalent and robust transcriptome/proteome expression phenotypes.", "authors": [{"family": "Hausmann", "given": "Annika", "initials": "A", "orcid": "0000-0001-8852-3444", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39.json"}}, {"family": "Russo", "given": "Giancarlo", "initials": "G"}, {"family": "Grossmann", "given": "Jonas", "initials": "J"}, {"family": "Z\u00fcnd", "given": "Mirjam", "initials": "M"}, {"family": "Schwank", "given": "Gerald", "initials": "G"}, {"family": "Aebersold", "given": "Ruedi", "initials": "R"}, {"family": "Liu", "given": "Yansheng", "initials": "Y"}, {"family": "Sellin", "given": "Mikael E", "initials": "ME", "orcid": "0000-0002-8355-0803", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/559c18ec87d64318a0afc6267ea879e2.json"}}, {"family": "Hardt", "given": "Wolf-Dietrich", "initials": "WD", "orcid": "0000-0002-9892-6420", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1049556a73b84d258e26a84382fe5870.json"}}], "type": "journal article", "published": "2020-06-00", "journal": {"title": "Cell. Microbiol.", "issn": "1462-5822", "issn-l": "1462-5814", "volume": "22", "issue": "6", "pages": "e13191"}, "abstract": "Intestinal epithelial organoids established from gut tissue have become a widely used research tool. However, it remains unclear how environmental cues, divergent microbiota composition and other sources of variation before, during and after establishment confound organoid properties, and how these properties relate to the original tissue. While environmental influences cannot be easily addressed in human organoids, mice offer a controlled assay-system. Here, we probed the effect of donor microbiota differences, previously identified as a confounding factor in murine in vivo studies, on organoids. We analysed the proteomes and transcriptomes of primary organoid cultures established from two colonised and one germ-free mouse colony of C57BL/6J genetic background, and compared them to their tissue of origin and commonly used cell lines. While an imprint of microbiota-exposure was observed on the proteome of epithelial samples, the long-term global impact of donor microbiota on organoid expression patterns was negligible. Instead, stochastic culture-to-culture differences accounted for a moderate variability between independently established organoids. Integration of transcriptome and proteome datasets revealed an organoid-typic expression signature comprising 14 transcripts and 10 proteins that distinguished organoids across all donors from murine epithelial cell lines and fibroblasts and closely mimicked expression patterns in the gut epithelium. This included the inflammasome components ASC, Naip1-6, Nlrc4 and Caspase-1, which were highly expressed in all organoids compared to the reference cell line m-ICc12 or mouse embryonic fibroblasts. Taken together, these results reveal that the donor microbiota has little effect on the organoid phenotype and suggest that organoids represent a more suitable culture model than immortalised cell lines, in particular for studies of intestinal epithelial inflammasomes.", "doi": "10.1111/cmi.13191", "pmid": "32068945", "labels": {"Mikael Sellin": "", "SciLifeLab Fellow": ""}, "xrefs": [{"db": "pmc", "key": "PMC7317401"}], "notes": [], "created": "2020-11-24T14:43:10.135Z", "modified": "2026-09-23T10:24:49.059Z"}, {"entity": "publication", "iuid": "e34e74a1e3ba4a2294331f3a4a860815", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/e34e74a1e3ba4a2294331f3a4a860815.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/e34e74a1e3ba4a2294331f3a4a860815"}}, "title": "Inflammation boosts bacteriophage transfer between Salmonella spp.", "authors": [{"family": "Diard", "given": "M\u00e9d\u00e9ric", "initials": "M", "orcid": "0000-0003-0851-4391", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6498d177bd1b4677b061ba9297cfe3d7.json"}}, {"family": "Bakkeren", "given": "Erik", "initials": "E", "orcid": "0000-0001-7970-7890", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/374cea304e9d49129f59d95dfe72b72e.json"}}, {"family": "Cornuault", "given": "Jeffrey K", "initials": "JK", "orcid": "0000-0001-8790-128X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/075cc48b7f144c708e16542d294a4577.json"}}, {"family": "Moor", "given": "Kathrin", "initials": "K", "orcid": "0000-0002-2799-3837", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a1f2f5c3572248e283cd8b0840e08be9.json"}}, {"family": "Hausmann", "given": "Annika", "initials": "A", "orcid": "0000-0001-8852-3444", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0048a8661d44d5e929f1724cded7b39.json"}}, {"family": "Sellin", "given": "Mikael E", "initials": "ME"}, {"family": "Loverdo", "given": "Claude", "initials": "C", "orcid": "0000-0002-0888-1717", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c6d208b2e4f244468904df8b2c6686ce.json"}}, {"family": "Aertsen", "given": "Abram", "initials": "A"}, {"family": "Ackermann", "given": "Martin", "initials": "M"}, {"family": "De Paepe", "given": "Marianne", "initials": "M", "orcid": "0000-0002-1076-9433", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e5fb594769dc4e7ba301279050a31d4f.json"}}, {"family": "Slack", "given": "Emma", "initials": "E", "orcid": "0000-0002-2473-1145", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d809599ee0dd4eb1b06ddf1ca6d51d09.json"}}, {"family": "Hardt", "given": "Wolf-Dietrich", "initials": "WD", "orcid": "0000-0002-9892-6420", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1049556a73b84d258e26a84382fe5870.json"}}], "type": "journal article", "published": "2017-03-17", "journal": {"title": "Science (New York, N.Y.)", "issn": "1095-9203", "issn-l": "0036-8075", "volume": "355", "issue": "6330", "pages": "1211-1215"}, "abstract": "Bacteriophage transfer (lysogenic conversion) promotes bacterial virulence evolution. There is limited understanding of the factors that determine lysogenic conversion dynamics within infected hosts. A murine Salmonella Typhimurium (STm) diarrhea model was used to study the transfer of SopE\u03a6, a prophage from STm SL1344, to STm ATCC14028S. Gut inflammation and enteric disease triggered >55% lysogenic conversion of ATCC14028S within 3 days. Without inflammation, SopE\u03a6 transfer was reduced by up to 105-fold. This was because inflammation (e.g., reactive oxygen species, reactive nitrogen species, hypochlorite) triggers the bacterial SOS response, boosts expression of the phage antirepressor Tum, and thereby promotes free phage production and subsequent transfer. Mucosal vaccination prevented a dense intestinal STm population from inducing inflammation and consequently abolished SopE\u03a6 transfer. Vaccination may be a general strategy for blocking pathogen evolution that requires disease-driven transfer of temperate bacteriophages.", "doi": "10.1126/science.aaf8451", "pmid": "28302859", "labels": {"Affiliated researcher": "", "Mikael Sellin": "", "SciLifeLab Fellow": ""}, "xrefs": [{"db": "pii", "key": "355/6330/1211"}], "notes": [], "created": "2018-12-03T14:42:45.748Z", "modified": "2026-09-23T06:43:49.051Z"}]}