ArticleInfection and immunity2008
Caspase-1 activation in macrophages infected with Yersinia pestis KIM requires the type III secretion system effector YopJ.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 78 citations in OpenAlex.
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- Effects of siRNA silencing on the susceptibility of the fish cell line CHSE-214 to Yersinia ruckeri.Veterinary research · 2020Article
- Difference in Strain Pathogenicity of Septicemic Yersinia pestis Infection in a TLR2Infection and immunity · 2020Article
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- Gain-of-Function Analysis Reveals Important Virulence Roles for the Yersinia pestis Type III Secretion System Effectors YopJ, YopT, and YpkA.Infection and immunity · 2018Article
- Induction of Type I Interferon through a Noncanonical Toll-Like Receptor 7 Pathway during Yersinia pestis Infection.Infection and immunity · 2017Article
- Bacterial secretion systems and regulation of inflammasome activation.Journal of leukocyte biology · 2017Review
- Cell-Extrinsic TNF Collaborates with TRIF Signaling To Promote Yersinia-Induced Apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Manipulation of Interleukin-1β and Interleukin-18 Production by Yersinia pestis Effectors YopJ and YopM and Redundant Impact on Virulence.The Journal of biological chemistry · 2016Article
- Uncovering an Important Role for YopJ in the Inhibition of Caspase-1 in Activated Macrophages and Promoting Yersinia pseudotuberculosis Virulence.Infection and immunity · 2016Article
- Yersinia type III effectors perturb host innate immune responses.World journal of biological chemistry · 2016Review
- Human caspase-4 mediates noncanonical inflammasome activation against gram-negative bacterial pathogens.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Macrophage cell death upon intracellular bacterial infection.Macrophage · 2015Article
- Yersinia pestis activates both IL-1β and IL-1 receptor antagonist to modulate lung inflammation during pneumonic plague.PLoS pathogens · 2015Article
- Gene silencing of non-obese diabetic receptor family (NLRP3) protects against the sepsis-induced hyper-bile acidaemia in a rat model.Clinical and experimental immunology · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Pathogenic Yersinia species utilize a type III secretion system (T3SS) to translocate effectors called Yersinia outer proteins (Yops) into infected host cells. Previous studies demonstrated a role for effector Yops in the inhibition of caspase-1-mediated cell death and secretion of interleukin-1beta (IL-1beta) in naïve macrophages infected with Yersinia enterocolitica. Naïve murine macrophages were infected with a panel of different Yersinia pestis and Yersinia pseudotuberculosis strains to determine whether Yops of these species inhibit caspase-1 activation. Cell death was measured by release of lactate dehydrogenase (LDH), and enzyme-linked immunosorbent assay for secreted IL-1beta was used to measure caspase-1 activation. Surprisingly, isolates derived from the Y. pestis KIM strain (e.g., KIM5) displayed an unusual ability to activate caspase-1 and kill infected macrophages compared to other Y. pestis and Y. pseudotuberculosis strains tested. Secretion of IL-1beta following KIM5 infection was reduced in caspase-1-deficient macrophages compared to wild-type macrophages. However, release of LDH was not reduced in caspase-1-deficient macrophages, indicating that cell death occurred independently of caspase-1. Analysis of KIM-derived strains defective for production of functional effector or translocator Yops indicated that translocation of catalytically active YopJ into macrophages was required for caspase-1 activation and cell death. Release of LDH and secretion of IL-1beta were not reduced when actin polymerization was inhibited in KIM5-infected macrophages, indicating that extracellular bacteria translocating YopJ could trigger cell death and caspase-1 activation. This study uncovered a novel role for YopJ in the activation of caspase-1 in macrophages.
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