Interferon Consensus Sequence Binding Protein Confers Resistance against<i>Yersinia enterocolitica</i>

Hein, Joachim; Kempf, Volkhard A. J.; Diebold, Joachim; Bücheler, Nicole; Preger, Sonja; Horak, Ivan D.; Sing, Andreas; Kramer, Uwe; Autenrieth, Ingo B.

doi:10.1128/iai.68.3.1408-1417.2000

Cited by 36 publications

(27 citation statements)

References 79 publications

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“…In addition, we were interested in characterizing and quantifying critical molecular and cellular components of the immune response following an oral Y. enterocolitica infection in tissues commonly colonized following an oral infection. The results from our Th1-Th2 cytokine analysis confirm observations made by other researchers that a Th1 environment, with high levels of IFN-␥ and low levels of IL-4 and IL-5, predominates during a Y. enterocolitica infection (10,12,27). We found this to be true in PP, MLN, and spleens of all mouse strains.…”

Section: Discussionsupporting

confidence: 80%

“…Studies initiated by Autenrieth and followed up on by Bohn and Autenrieth have demonstrated several potential mechanisms to explain the increased resistance of C57BL/6 mice to BALB/c mice in an i.v.-administered Y. enterocolitica infection model (2,3,(9)(10)(11)(12)27). Their work demonstrates that as an i.v.-administered infection progresses, C57BL/6 mouse spleens mount a more pronounced inflammatory response than do BALB/c mouse spleens.…”

Section: Discussionmentioning

confidence: 99%

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Characterization of OralYersinia enterocoliticaInfection in Three Different Strains of Inbred Mice

Handley¹,

Dube²,

Revell³

et al. 2004

Infect Immun

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Several studies have highlighted differences in the resistances of various mouse strains to intravenous (i.v.) infection with Yersinia enterocolitica. In particular, differences in resistance and immunological response between BALB/c and C57BL/6 mouse strains have been determined. Following i.v infection, C57BL/6 mice are more resistant to Y. enterocolitica than are BALB/c mice. However, because Y. enterocolitica is typically a food-borne pathogen, the oral route of infection more accurately reflects the natural route of infection. Therefore, it was of interest to ascertain if the differences in resistance between mouse strains observed for an i.v. infection can be recapitulated following an oral infection. C57BL/6j, BALB/cj, and 129X1/Svj mouse strains presented no differences in 50% lethal dose (LD 50 ) following oral infection with Y. enterocolitica. Subsequent analysis of cytokine levels, bacterial colonization and immune cell populations following oral infection confirmed characteristics previously described following i.v. Y. enterocolitica infection. All tissues analyzed from each mouse strain demonstrated a polarized Th1 cytokine profile and inflammatory cell influx throughout a 7-day course of infection. This immune response was present in all tissues and increased as bacterial colonization progressed. The lack of a differing LD 50 phenotype and common trends in immunological response among the three mouse strains tested suggests that oral infection is a useful model for studying the host response to Y. enterocolitica infection.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Characterization of OralYersinia enterocoliticaInfection in Three Different Strains of Inbred Mice

Handley¹,

Dube²,

Revell³

et al. 2004

Infect Immun

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“…Furthermore, ICSBP Ϫ/Ϫ macrophages are functionally defective. They do not produce sufficient amounts of reactive oxygen intermediates upon microbial challenges and fail to express IL-12, making these mice highly susceptible to infections (13)(14)(15)(16)(17)(18). Scheller et al (19) provided evidence that these abnormalities are traced to a defect in myeloid progenitor cells.…”

Section: Ifn Consensus Sequence Binding Protein/ifn Regulatory Factormentioning

confidence: 99%

IFN Consensus Sequence Binding Protein/IFN Regulatory Factor-8 Guides Bone Marrow Progenitor Cells Toward the Macrophage Lineage

Tsujimura

Nagamura‐Inoue

Tamura

et al. 2002

The Journal of Immunology

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IFN consensus sequence binding protein (ICSBP; IFN regulatory factor-8) is a transcription factor of the IFN regulatory factor family. Disruption of this gene results in a leukemia-like disease in mice. To investigate the role of ICSBP in myeloid cell development, lineage marker-negative (Lin−) bone marrow progenitor cells were purified from ICSBP+/+ and ICSBP−/− mice and tested for gene expression and colony-forming ability. ICSBP was expressed in Lin− progenitor cells, and its levels were markedly increased by IFN-γ. The colony-forming potential of ICSBP−/− progenitor cells was grossly abnormal, as they gave rise to a disproportionately high number of granulocyte colonies and many fewer macrophage colonies. IFN-γ inhibited colony formation, while promoting macrophage maturation in ICSBP+/+ cells. In contrast, the effects of IFN-γ were completely absent in ICSBP−/− progenitors. By retrovirus transduction we tested whether reintroduction of ICSBP restores a normal colony-forming potential in −/− progenitor cells. The wild-type ICSBP, but not transcriptionally defective mutants, corrected abnormal colony formation by increasing macrophage colonies and decreasing granulocyte colonies. Taken together, ICSBP plays a critical role in myeloid cell development by controlling lineage selection and is indispensable for IFN-γ-dependent modulation of progenitor cell maturation.

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“…The loss of IFN-␥ expression in the Y. pestis KIM5-infected mice may have contributed to the histopathology in the livers and spleens of these animals. A large body of evidence documents the importance of IFN-␥ production in the formation of granulomas (1,2,8,11,19,35,39). With the loss of IFN-␥ expression in the mice infected with the parent Y. pestis, macrophage activation and granuloma formation were prevented.…”

Section: Previous Studies In Balb/c Mice Have Shown That Yopmmentioning

confidence: 99%

The Plague Virulence Protein YopM Targets the Innate Immune Response by Causing a Global Depletion of NK Cells

et al. 2004

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Interferon Consensus Sequence Binding Protein Confers Resistance againstYersinia enterocolitica

Cited by 36 publications

References 79 publications

Characterization of OralYersinia enterocoliticaInfection in Three Different Strains of Inbred Mice

Characterization of OralYersinia enterocoliticaInfection in Three Different Strains of Inbred Mice

IFN Consensus Sequence Binding Protein/IFN Regulatory Factor-8 Guides Bone Marrow Progenitor Cells Toward the Macrophage Lineage

The Plague Virulence Protein YopM Targets the Innate Immune Response by Causing a Global Depletion of NK Cells

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