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Titolo:
A novel function of InIB from Listeria monocytogenes: activation of NF-kappa B in J774 macrophages
Autore:
Mansell, A; Braun, L; Cossart, P; ONeill, LAJ;
Indirizzi:
Univ Dublin Trinity Coll, Dept Biochem, Dublin 2, Ireland Univ Dublin Trinity Coll Dublin Ireland 2 ept Biochem, Dublin 2, Ireland Univ Dublin Trinity Coll, Inst Biotechnol, Dublin 2, Ireland Univ Dublin Trinity Coll Dublin Ireland 2 Biotechnol, Dublin 2, Ireland Inst Pasteur, Unite Interact Bacteries Cellules, F-75724 Paris, France Inst Pasteur Paris France F-75724 teries Cellules, F-75724 Paris, France
Titolo Testata:
CELLULAR MICROBIOLOGY
fascicolo: 2, volume: 2, anno: 2000,
pagine: 127 - 136
SICI:
1462-5814(200004)2:2<127:ANFOIF>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERNALIN MULTIGENE FAMILY; ACTIN-BASED MOVEMENT; RICH REPEAT REGION; MAMMALIAN-CELLS; PHOSPHOINOSITIDE 3-KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; SIGNAL-TRANSDUCTION; INDUCED APOPTOSIS; SURFACE PROTEIN; E-CADHERIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: O'Neill, LAJ Univ Dublin Trinity Coll, Dept Biochem, Dublin 2, Ireland Univ Dublin Trinity Coll Dublin Ireland 2 Dublin 2, Ireland
Citazione:
A. Mansell et al., "A novel function of InIB from Listeria monocytogenes: activation of NF-kappa B in J774 macrophages", CELL MICROB, 2(2), 2000, pp. 127-136

Abstract

Listeria monocytogenes causes a pro-inflammatory response on adhesion to macrophages. Upregulation of inflammation genes involves the transcription factor NF-kappa B. Several components of L. monocytogenes, including lipoteichoic acid (LTA), phospholipases and listeriolysin O (LLO), have since beenshown to mediate NF-kappa B activation. Here, we report that purified recombinant InlB, but not internalin (InlA), is a potent activator of NF-kappa B in the mouse macrophage-like cell line J774. Expression of InlB in Listeria innocua enhances its ability to activate NF-kappa B, while deletion of InlB from L. monocytogenes marginally decreases its effect on NF-kappa B, possibly because of the presence of NF-kappa B activators such as LTA and LLO. The effect correlates with the rapid degradation of I kappa B alpha, a sustained degradation of I kappa B beta and increases in tumour necrosis factor alpha (TNF-alpha) and interleukin (IL) 6 production, two cytokines controlled by NF-kappa B. Using a series of anti-InlB monoclonal antibodies and domains of InlB, NF-kappa B activation was shown to be dependent upon the N-terminal 213-amino-acid leucine-rich repeat (LRR) domain of InlB, recentlydemonstrated to be responsible for InlB-mediated L. monocytogenes invasionand phosphoinositide-3 (PI-3) kinase activation. The effect of InlB was blocked by PI-3 kinase inhibitors, indicating the involvement of PI-3 kinase in this response. This report thus illustrates that InlB not only promotes invasion, but also contributes to the macrophage pro-inflammatory response.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 08:12:02