{"doi":"10.1128/iai.01344-10","title":"IglG and IglI of the Francisella Pathogenicity Island Are Important Virulence Determinants of Francisella tularensis LVS","abstract":"<jats:title>ABSTRACT</jats:title>\n          <jats:p>\n            The Gram-negative bacterium\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella tularensis</jats:named-content>\n            is the causative agent of tularemia, a disease intimately associated with the multiplication of the bacterium within host macrophages. This in turn requires the expression of\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella</jats:named-content>\n            pathogenicity island (FPI) genes, believed to encode a type VI secretion system. While the exact functions of many of the components have yet to be revealed, some have been found to contribute to the ability of\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella</jats:named-content>\n            to cause systemic infection in mice as well as to prevent phagolysosomal fusion and facilitate escape into the host cytosol. Upon reaching this compartment, the bacterium rapidly multiplies, inhibits activation of the inflammasome, and ultimately causes apoptosis of the host cell. In this study, we analyzed the contribution of the FPI-encoded proteins IglG, IglI, and PdpE to the aforementioned processes in\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">F. tularensis</jats:named-content>\n            LVS. The Δ\n            <jats:italic>pdpE</jats:italic>\n            mutant behaved similarly to the parental strain in all investigated assays. In contrast, Δ\n            <jats:italic>iglG</jats:italic>\n            and Δ\n            <jats:italic>iglI</jats:italic>\n            mutants, although they were efficiently replicating in J774A.1 cells, both exhibited delayed phagosomal escape, conferred a delayed activation of the inflammasome, and exhibited reduced cytopathogenicity as well as marked attenuation in the mouse model. Thus, IglG and IglI play key roles for modulation of the intracellular host response and also for the virulence of\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">F. tularensis</jats:named-content>\n            .\n          </jats:p>","journal":"Infection and Immunity","year":2011,"id":628827,"datarank":0.5837730447165941,"base_score":3.8918202981106265,"endowment":3.8918202981106265,"self_citation_contribution":0.5837730447165941,"citation_network_contribution":0.0,"self_endowment_contribution":0.5837730447165941,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":48,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1628300,"name":"Moa Lavander","orcid":null,"position":1,"is_corresponding":false},{"id":505620,"name":"Lena Meyer","orcid":null,"position":2,"is_corresponding":false},{"id":766881,"name":"Anders Sjöstedt","orcid":"0000-0002-0768-8405","position":3,"is_corresponding":false},{"id":968918,"name":"Jeanette E. Bröms","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"IglG and IglI of the Francisella Pathogenicity Island Are Important Virulence Determinants of Francisella tularensis LVS","abstract":"<jats:title>ABSTRACT</jats:title>\n          <jats:p>\n            The Gram-negative bacterium\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella tularensis</jats:named-content>\n            is the causative agent of tularemia, a disease intimately associated with the multiplication of the bacterium within host macrophages. This in turn requires the expression of\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella</jats:named-content>\n            pathogenicity island (FPI) genes, believed to encode a type VI secretion system. While the exact functions of many of the components have yet to be revealed, some have been found to contribute to the ability of\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Francisella</jats:named-content>\n            to cause systemic infection in mice as well as to prevent phagolysosomal fusion and facilitate escape into the host cytosol. Upon reaching this compartment, the bacterium rapidly multiplies, inhibits activation of the inflammasome, and ultimately causes apoptosis of the host cell. In this study, we analyzed the contribution of the FPI-encoded proteins IglG, IglI, and PdpE to the aforementioned processes in\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">F. tularensis</jats:named-content>\n            LVS. The Δ\n            <jats:italic>pdpE</jats:italic>\n            mutant behaved similarly to the parental strain in all investigated assays. In contrast, Δ\n            <jats:italic>iglG</jats:italic>\n            and Δ\n            <jats:italic>iglI</jats:italic>\n            mutants, although they were efficiently replicating in J774A.1 cells, both exhibited delayed phagosomal escape, conferred a delayed activation of the inflammasome, and exhibited reduced cytopathogenicity as well as marked attenuation in the mouse model. Thus, IglG and IglI play key roles for modulation of the intracellular host response and also for the virulence of\n            <jats:named-content xmlns:xlink=\"http://www.w3.org/1999/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">F. tularensis</jats:named-content>\n            .\n          </jats:p>","is_dataset_classified":null,"base_score":3.8918202981106265,"endowment":3.8918202981106265,"datacite_reuse_total":0,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"21690239","pmcid":"PMC3165494","openalex_id":"https://openalex.org/W2169497969","authors":[],"funders":[],"total_grants":0,"fwci":2.6763,"citation_percentile":0.90889774,"influential_citations":0,"citation_trend":[{"year":2012,"count":7},{"year":2013,"count":8},{"year":2014,"count":5},{"year":2015,"count":4},{"year":2016,"count":6},{"year":2017,"count":3},{"year":2018,"count":2},{"year":2019,"count":1},{"year":2020,"count":4},{"year":2021,"count":1},{"year":2023,"count":1},{"year":2024,"count":2},{"year":2026,"count":2}],"oa_status":"green","license":"other-oa","oa_locations":[{"url":"http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-83830","host_type":"repository"},{"url":"http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-83830","host_type":"repository"},{"url":"https://journals.asm.org/doi/pdf/10.1128/IAI.01344-10","host_type":"publisher"},{"url":"https://doi.org/10.1128/iai.01344-10","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21690239","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/3165494","host_type":"repository"}],"fields_of_study":["Bacillus and Francisella bacterial research","Viral Infections and Outbreaks Research","Yersinia bacterium, plague, ectoparasites research","Animals","Apoptosis","Bacterial Proteins","Bacterial Secretion Systems","Cell Line","Francisella tularensis","Gene Expression Regulation, Bacterial","Genes, Bacterial","Genomic Islands","Inflammasomes","Macrophages","Mice","Mice, Inbred C57BL","Microscopy, Electron, Transmission","Phagocytosis","Phagosomes","Polymerase Chain Reaction","Sequence Deletion","Tularemia","Virulence Factors"],"mesh_terms":["Animals","Bacterial Proteins","Cell Line","Francisella tularensis","Genes, Bacterial","Macrophages","Mice, Inbred C57BL","Phagocytosis","Phagosomes","Tularemia","Gene Expression Regulation, Bacterial","Polymerase Chain Reaction","Apoptosis","Sequence Deletion","Virulence Factors","Genomic Islands","Microscopy, Electron, Transmission","Mice","Inflammasomes","Bacterial Secretion Systems"],"keywords":["Francisella tularensis","Tularemia","Francisella","Biology","Virulence","Microbiology","Pathogenicity island","Bacteria","Intracellular parasite","Secretion","Mutant","Pyroptosis","Inflammasome","Intracellular","Virology","Gene","Cell biology","Genetics","Immunology","Inflammation"],"sdg_mappings":[{"sdg_number":0,"sdg_label":"Life below water"}],"linked_datasets":[],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-05T15:16:56.202536Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}