YopJ-Promoted Cytotoxicity and Systemic Colonization Are Associated with High Levels of Murine Interleukin-18, Gamma Interferon, and Neutrophils in a Live Vaccine Model of<i>Yersinia pseudotuberculosis</i>Infection

Zhang, Yue; Bliska, James B.

doi:10.1128/iai.00094-10

Cited by 28 publications

(46 citation statements)

References 76 publications

(124 reference statements)

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“…Y. pestis strain KIM D27, used for protection studies, was described previously (66). The KIM D27 strain lacks the pgm locus and is exempt from select-agent guidelines.…”

Section: Methodsmentioning

confidence: 99%

“…The Y. pseudotuberculosis strains used in this study are the serogroup O:1 strain 32777 (66) and its derivative, mE, which carries the catalytic inactive YopE(R144A) protein.…”

Section: Methodsmentioning

confidence: 99%

“…have been utilized as experimental live vaccines in mouse infection models to prime protective immunity against virulent yersiniae and other pathogens (9,42,48,58). For example, it has been shown that mice that survive infection with wildtype (wt) or attenuated Y. pseudotuberculosis are well protected against challenge with virulent Y. pestis (12,47,54,66). In addition, the plasmid-encoded T3SS has been utilized for delivery of heterologous CD4 or CD8 antigens by live attenuated Y. pseudotuberculosis and Y. enterocolitica carrier strains (30, 43-45, 56, 58, 61).…”

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confidence: 99%

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A Protective Epitope in Type III Effector YopE Is a Major CD8 T Cell Antigen during Primary Infection with Yersinia pseudotuberculosis

et al. 2012

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“…Y. pestis strain KIM D27, used for protection studies, was described previously (66). The KIM D27 strain lacks the pgm locus and is exempt from select-agent guidelines.…”

Section: Methodsmentioning

confidence: 99%

“…The Y. pseudotuberculosis strains used in this study are the serogroup O:1 strain 32777 (66) and its derivative, mE, which carries the catalytic inactive YopE(R144A) protein.…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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A Protective Epitope in Type III Effector YopE Is a Major CD8 T Cell Antigen during Primary Infection with Yersinia pseudotuberculosis

et al. 2012

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“…Mice were acclimated for 1 week after arrival and deprived of food and water for 6 h before starting experiments. The median lethal dose (LD 50 ) of the Y. pseudotuberculosis strains in mice was determined according to previous procedures with certain modifications (73)(74)(75). Overnight cultures of bacteria were grown at 26°C in LB supplemented with 0.05% arabinose when needed.…”

Section: Table 2 Primers Used In This Workmentioning

confidence: 99%

LcrV Delivered via Type III Secretion System of Live Attenuated Yersinia pseudotuberculosis Enhances Immunogenicity against Pneumonic Plague

et al. 2014

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“…Y. pestis can induce cell death in macrophages and dendritic cells via the type III secretion system (T3SS) effector Yersinia outer protein J (YopJ; YopP in Yersinia enterocolitica), although it is unclear whether this is entirely by apoptosis (11,12). All human-pathogenic Yersiniae (Y. pestis, Yersinia pseudotuberculosis, and Y. enterocolitica) harbor cytotoxic properties toward host cells, and YopJ production is associated with cell death in vivo and in vitro (13)(14)(15)(16). YopJ-mediated inhibition of NF-κB by acetylation of Inhibitor of κB Kinase β (IKKβ), MAP kinase kinases, and TAK1 may modulate macrophage death via effects on inflammatory and prosurvival signals (2,(17)(18)(19)(20)(21).…”

mentioning

confidence: 99%

Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death

Weng

Marty-Roix

Ganesan

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

263

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A number of pathogens cause host cell death upon infection, and Yersinia pestis, infamous for its role in large pandemics such as the "Black Death" in medieval Europe, induces considerable cytotoxicity. The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effector Yersinia outer protein J (YopJ), is minimally affected by the absence of caspase-1, caspase-11, Fas ligand, and TNF. Caspase-8 is known to mediate apoptotic death in response to infection with several viruses and to regulate programmed necrosis (necroptosis), but its role in bacterially induced cell death is poorly understood. Here we provide genetic evidence for a receptor-interacting protein (RIP) kinasecaspase-8-dependent macrophage apoptotic death pathway after infection with Y. pestis, influenced by Toll-like receptor 4-TIR-domain-containing adapter-inducing interferon-β (TLR4-TRIF). Interestingly, macrophages lacking either RIP1, or caspase-8 and RIP3, also had reduced infection-induced production of IL-1β, IL-18, TNF, and IL-6; impaired activation of the transcription factor NF-κB; and greatly compromised caspase-1 processing. Cleavage of the proform of caspase-1 is associated with triggering inflammasome activity, which leads to the maturation of IL-1β and IL-18, cytokines important to host responses against Y. pestis and many other infectious agents. Our results identify a RIP1-caspase-8/RIP3-dependent caspase-1 activation pathway after Y. pestis challenge. Mice defective in caspase-8 and RIP3 were also highly susceptible to infection and displayed reduced proinflammatory cytokines and myeloid cell death. We propose that caspase-8 and the RIP kinases are key regulators of macrophage cell death, NF-κB and inflammasome activation, and host resistance after Y. pestis infection.

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YopJ-Promoted Cytotoxicity and Systemic Colonization Are Associated with High Levels of Murine Interleukin-18, Gamma Interferon, and Neutrophils in a Live Vaccine Model ofYersinia pseudotuberculosisInfection

Cited by 28 publications

References 76 publications

A Protective Epitope in Type III Effector YopE Is a Major CD8 T Cell Antigen during Primary Infection with Yersinia pseudotuberculosis

A Protective Epitope in Type III Effector YopE Is a Major CD8 T Cell Antigen during Primary Infection with Yersinia pseudotuberculosis

LcrV Delivered via Type III Secretion System of Live Attenuated Yersinia pseudotuberculosis Enhances Immunogenicity against Pneumonic Plague

Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death

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