ArticleInfection and immunity2009
Francisella tularensis induces extensive caspase-3 activation and apoptotic cell death in the tissues of infected mice.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 77 citations in OpenAlex.
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- Non-Canonical Inflammasome Pathway: The Role of Cell Death and Inflammation in Ehrlichiosis.Cells · 2023Review
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- PGRS Domain of Rv0297 ofFrontiers in cellular and infection microbiology · 2020Article
- Contributions of TolC Orthologs toInfection and immunity · 2019Article
- Innate Immune Recognition: An Issue More Complex Than Expected.Frontiers in cellular and infection microbiology · 2019Review
- Temporal Manipulation of Mitochondrial Function by Virulent Francisella tularensis To Limit Inflammation and Control Cell Death.Infection and immunity · 2018Article
- Deletion of the Major Facilitator Superfamily TransporterInfection and immunity · 2018Article
- Complement Receptor 3-Mediated Inhibition of Inflammasome Priming by Ras GTPase-Activating Protein DuringFrontiers in immunology · 2018Article
- Hematopoietic MyD88 and IL-18 are essential for IFN-γ-dependent restriction of type AJournal of leukocyte biology · 2017Article
- Complement C3 as a Prompt for Human Macrophage Death during Infection with Francisella tularensis Strain SCHU S4.Infection and immunity · 2017Article
- Article
- Differential roles of caspase-1 and caspase-11 in infection and inflammation.Scientific reports · 2017Article
- The Natural History of Pneumonic Tularemia in Female Fischer 344 Rats after Inhalational Exposure to Aerosolized Francisella tularensis Subspecies tularensis Strain SCHU S4.The American journal of pathology · 2017Article
- Article
- Differential MicroRNA Analyses ofInternational journal of genomics · 2017Article
- Necroptotic debris including damaged mitochondria elicits sepsis-like syndrome during late-phase tularemia.Cell death discovery · 2017Article
- Inflammasome-Independent NLRP3 Restriction of a Protective Early Neutrophil Response to Pulmonary Tularemia.PLoS pathogens · 2016Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Although Francisella tularensis subsp. tularensis is known to cause extensive tissue necrosis, the pathogenesis of tissue injury has not been elucidated. To characterize cell death in tularemia, C57BL/6 mice were challenged by the intranasal route with type A F. tularensis, and the pathological changes in infected tissues were characterized over the next 4 days. At 3 days postinfection, well-organized inflammatory infiltrates developed in the spleen and liver following the spread of infection from the lungs. By the next day, extensive cell death, characterized by the presence of pyknotic cells containing double-strand DNA breaks, was apparent throughout these inflammatory foci. Cell death was not mediated by activated caspase-1, as has been reported for cells infected with other Francisella subspecies. Mouse macrophages and dendritic cells that had been stimulated with type A F. tularensis did not release interleukin-18 in vitro, a response that requires the activation of procaspase-1. Dying cells within type A F. tularensis-infected tissues expressed activated caspase-3 but very little activated caspase-1. When caspase-1-deficient mice were challenged with type A F. tularensis, pathological changes, including extensive cell death, were similar to those seen in infected wild-type mice. In contrast, type A F. tularensis-infected caspase-3-deficient mice showed much less death among their F4/80+ spleen cells than did infected wild-type mice, and they retained the ability to express tumor necrosis factor alpha and inducible NO synthase. These findings suggest that type A F. tularensis induces caspase-3-dependent macrophage apoptosis, resulting in the loss of potentially important innate immune responses to the pathogen.
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