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Titolo:
Interferon consensus sequence binding protein confers resistance against Yersinia enterocolitica
Autore:
Hein, J; Kempf, VAJ; Diebold, J; Bucheler, N; Preger, S; Horak, I; Sing, A; Kramer, U; Autenrieth, IB;
Indirizzi:
Univ Munich, Max Von Pettenkofer Inst Hyg & Med Microbiol, Munich, GermanyUniv Munich Munich Germany er Inst Hyg & Med Microbiol, Munich, Germany Univ Munich, Inst Pathol, Munich, Germany Univ Munich Munich GermanyUniv Munich, Inst Pathol, Munich, Germany Forschungsinst Mol Pharmakol, Abt Mol Genet, Berlin, Germany Forschungsinst Mol Pharmakol Berlin Germany Mol Genet, Berlin, Germany
Titolo Testata:
INFECTION AND IMMUNITY
fascicolo: 3, volume: 68, anno: 2000,
pagine: 1408 - 1417
SICI:
0019-9567(200003)68:3<1408:ICSBPC>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; REGULATORY FACTOR FAMILY; IFN-GAMMA PRODUCTION; NF-KAPPA-B; TRANSCRIPTION FACTOR; IMMUNE-RESPONSES; MESSENGER-RNA; CELL-DEATH; IN-VIVO; VIRULENCE PLASMID;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
77
Recensione:
Indirizzi per estratti:
Indirizzo: Autenrieth, IB Univ Munich, Max Von Pettenkofer Inst, Pettenkoferstr 9A, D-80336 Munich, Germany Univ Munich Pettenkoferstr 9A Munich Germany D-80336 rmany
Citazione:
J. Hein et al., "Interferon consensus sequence binding protein confers resistance against Yersinia enterocolitica", INFEC IMMUN, 68(3), 2000, pp. 1408-1417

Abstract

Interferon consensus sequence binding protein (ICSBP)-deficient mice display enhanced susceptibility to intracellular pathogens. At least two distinct immunoregulatory defects are responsible for this phenotype. First, diminished production of reactive oxygen intermediates in macrophages results inimpaired intracellular killing of microorganisms. Second, defective early interleukin-12 (IL-12) production upon microbial challenge leads to a failure in gamma interferon (IFN-gamma) induction and subsequently in T helper Iimmune responses. Here, we investigated the role of ICSBP in resistance against the extracellular bacterium Yersinia enterocolitica. ICSBP-/- mice failed to produce IL-12 and IFN-gamma, but also IL-4, after Yersinia challenge. In addition, granuloma formation was highly disturbed in infected ICSBP-/- mice, leading to multiple necrotic abscesses in affected organs. Consequently, ICSBP-/- mite rapidly succumbed to acute Yersinia infection. In vitro treatment of spleen cells from ICSBP-/- mice with recombinant IL-12 (rIL-12) or rIL-18 in combination with a second stimulus resulted in IFN-gamma induction. In experimental therapy of infected ICSBP-/- mice, we observed that administration of rIL-12 induced IFN-gamma production which was associated with improved resistance to Yersinia. In contrast, treatment with rIL-18failed to enhance endogenous IFN-gamma production but nevertheless reducedbacterial burden in ICSBP-/- mice. Although cytokine therapy with rIL-12 or rIL-18 ameliorated the course of Yersinia infection in ICSBP-/- mice, both cytokines failed to completely restore impaired immunity. Taken together,the results indicate that the transcription factor ICSBP is essential for efficient host immune defense against Yersinia. These results are importantfor understanding the complex host immune responses in bacterial infections.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 14:23:27