Intestinal organoids model human responses to infection by commensal and Shiga toxin producing Escherichia coli
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{"title"=>"Intestinal organoids model human responses to infection by commensal and Shiga toxin producing Escherichia coli", "type"=>"journal", "authors"=>[{"first_name"=>"Sayali S.", "last_name"=>"Karve", "scopus_author_id"=>"54971257100"}, {"first_name"=>"Suman", "last_name"=>"Pradhan", "scopus_author_id"=>"57189505154"}, {"first_name"=>"Doyle V.", "last_name"=>"Ward", "scopus_author_id"=>"55464681600"}, {"first_name"=>"Alison A.", "last_name"=>"Weiss", "scopus_author_id"=>"7402247546"}], "year"=>2017, "source"=>"PLoS ONE", "identifiers"=>{"pui"=>"616783197", "sgr"=>"85020914748", "issn"=>"19326203", "pmid"=>"28614372", "scopus"=>"2-s2.0-85020914748", "doi"=>"10.1371/journal.pone.0178966", "isbn"=>"1111111111"}, "id"=>"4bcfd31c-ddcc-33f1-b85d-c5365263e602", "abstract"=>"Infection with Shiga toxin (Stx) producing Escherichia coli O157:H7 can cause the poten-tially fatal complication hemolytic uremic syndrome, and currently only supportive therapy is available. Lack of suitable animal models has hindered study of this disease. Induced human intestinal organoids (iHIOs), generated by in vitro differentiation of pluripotent stem cells, represent differentiated human intestinal tissue. We show that iHIOs with addition of human neutrophils can model E. coli intestinal infection and innate cellular responses. Com-mensal and O157:H7 introduced into the iHIO lumen replicated rapidly achieving high num-bers. Commensal E. coli did not cause damage, and were completely contained within the lumen, suggesting defenses, such as mucus production, can constrain non-pathogenic strains. Some O157:H7 initially co-localized with cellular actin. Loss of actin and epithelial integrity was observed after 4 hours. O157:H7 grew as filaments, consistent with activation of the bacterial SOS stress response. SOS is induced by reactive oxygen species (ROS), and O157:H7 infection increased ROS production. Transcriptional profiling (RNAseq) dem-onstrated that both commensal and O157:H7 upregulated genes associated with gastroin-testinal maturation, while infection with O157:H7 upregulated inflammatory responses, including interleukin 8 (IL-8). IL-8 is associated with neutrophil recruitment, and infection with O157:H7 resulted in recruitment of human neutrophils into the iHIO tissue.", "link"=>"http://www.mendeley.com/research/intestinal-organoids-model-human-responses-infection-commensal-shiga-toxin-producing-escherichia-col-3", "reader_count"=>31, "reader_count_by_academic_status"=>{"Unspecified"=>1, "Researcher"=>7, "Student > Doctoral Student"=>4, "Student > Ph. D. Student"=>8, "Other"=>1, "Student > Master"=>5, "Student > Bachelor"=>4, "Lecturer"=>1}, "reader_count_by_user_role"=>{"Unspecified"=>1, "Researcher"=>7, "Student > Doctoral Student"=>4, "Student > Ph. D. Student"=>8, "Other"=>1, "Student > Master"=>5, "Student > Bachelor"=>4, "Lecturer"=>1}, "reader_count_by_subject_area"=>{"Unspecified"=>2, "Environmental Science"=>1, "Biochemistry, Genetics and Molecular Biology"=>7, "Agricultural and Biological Sciences"=>9, "Medicine and Dentistry"=>3, "Pharmacology, Toxicology and Pharmaceutical Science"=>1, "Veterinary Science and Veterinary Medicine"=>1, "Chemistry"=>1, "Immunology and Microbiology"=>6}, "reader_count_by_subdiscipline"=>{"Medicine and Dentistry"=>{"Medicine and Dentistry"=>3}, "Chemistry"=>{"Chemistry"=>1}, "Immunology and Microbiology"=>{"Immunology and Microbiology"=>6}, "Agricultural and Biological Sciences"=>{"Agricultural and Biological Sciences"=>9}, "Biochemistry, Genetics and Molecular Biology"=>{"Biochemistry, Genetics and Molecular Biology"=>7}, "Unspecified"=>{"Unspecified"=>2}, "Environmental Science"=>{"Environmental Science"=>1}, "Pharmacology, Toxicology and Pharmaceutical Science"=>{"Pharmacology, Toxicology and Pharmaceutical Science"=>1}, "Veterinary Science and Veterinary Medicine"=>{"Veterinary Science and Veterinary Medicine"=>1}}, "reader_count_by_country"=>{"United Kingdom"=>1}, "group_count"=>0}

Scopus | Further Information

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Scopus
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2019-09-26 19:19:09 UTC
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https://api.elsevier.com/content/search/index:SCOPUS?query=DOI(10.1371%2Fjournal.pone.0178966)
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