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Titolo:
Effects of systemic immunogenic insults and circulating proinflammatory cytokines on the transcription of the inhibitory factor kappa B alpha within specific cellular populations of the rat brain
Autore:
Laflamme, N; Rivest, S;
Indirizzi:
CHU Laval, Res Ctr, Mol Endocrinol Lab, St Foy, PQ G1V 4G2, Canada CHU Laval St Foy PQ Canada G1V 4G2 crinol Lab, St Foy, PQ G1V 4G2, Canada Univ Laval, St Foy, PQ G1V 4G2, Canada Univ Laval St Foy PQ Canada G1V 4G2 niv Laval, St Foy, PQ G1V 4G2, Canada
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 1, volume: 73, anno: 1999,
pagine: 309 - 321
SICI:
0022-3042(199907)73:1<309:EOSIIA>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; CORTICOTROPIN-RELEASING FACTOR; CENTRAL-NERVOUS-SYSTEM; LPS BINDING-PROTEIN; MESSENGER-RNA; LIPOPOLYSACCHARIDE LPS; INTERLEUKIN-6 GENE; INTERLEUKIN-1-BETA-DEFICIENT MICE; INTRAVENOUS INTERLEUKIN-1; INFLAMMATORY RESPONSE;
Keywords:
blood vessels; circumventricular organs; endothelial cells; in situ hybridization histochemistry; inflammation; immunocytochemistry; lipopolysaccharide; proinflammatory cytokines; microglia; macrophages; septic shock; transcription factor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Rivest, S CHUG2,val, Res Ctr, Mol Endocrinol Lab, 2705 Blvd Laurier, St Foy, PQ G1V 4 CHU Laval 2705 Blvd Laurier St Foy PQ Canada G1V 4G2 y, PQ G1V 4
Citazione:
N. Laflamme e S. Rivest, "Effects of systemic immunogenic insults and circulating proinflammatory cytokines on the transcription of the inhibitory factor kappa B alpha within specific cellular populations of the rat brain", J NEUROCHEM, 73(1), 1999, pp. 309-321

Abstract

Expression of the inhibitory factor kappa B alpha (I kappa B alpha) reflects the activity of nuclear factor kappa B(NF-kappa B) and is a powerful tool to investigate the regulation of the transcription factor within the CNS. I kappa B alpha mRNA was evaluated in the rat brain by means of in situ hybridization following different immunogenic stimuli; i.e., intraperitoneal (i.p,) and intravenous (i.v.) lipopolysaccharide (LPS), i.v. recombinant rat interleukin ([L) 1 beta, IL-6, or tumor necrosis factor-alpha (TNF-alpha), and intramuscular (i.m.) turpentine injection, used here as a model of systemic localized inflammatory insult. Systemic LPS, IL-1 beta, and TNF-alpha caused a rapid and transient transcriptional activation of I kappa B alpha along the blood vessels of the entire brain; the signal was very intense 30-60 min after the i.v. injections and returned to undetectable levels from 2 to 12 h depending on the challenge, Double-labeling procedure provided the anatomical evidence that I kappa B alpha-expressing cells within the microvasculature were essentially of the endothelial type, as they were immunoreactive to the von Willebrand factor. Scattered small cells were also found across the brain of LPS-, IL-1 beta-, and TNF-alpha-injected rats at time 1-3 h, and microglial (OX-42)immunoreactive cells were positive for the transcript. Such expression within parenchymal microglia was nevertheless not observed in the brain following a localized and sterile inflammatory insult. indeed, i.m. turpentine administration stimulated I kappa B alpha transcription quite uniquely within the endothelium of the brain capillaries, aneffect that paralleled the swelling of the injection site and lasted up to24 h after the aggression. In contrast to these immunogenic challenges, i.v. IL-6 injection failed to activate the gene encoding I kappa B alpha in the rat brain. These results indicate that NF-kappa B may play a crucial role in specific cellular populations of the CNS to trigger transcription of immune-related genes and that I kappa B alpha resynthesis may act as a dynamic intracellular inhibitory feedback to avoid exaggeration of the response. It is possible that I kappa B alpha expression in cells of the blood-brainbarrier is a general mechanism that takes place during systemic inflammation, whereas the participation of NF-kappa B-related molecules within parenchymal cells of the CNS is solicited during more severe conditions such as blood sepsis and endotoxemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 15:05:09