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Titolo:
Regulation of the gene encoding the monocyte chemoattractant protein 1 (MCP-1) in the mouse and rat brain in response to circulating LPS and proinflammatory cytokines
Autore:
Thibeault, I; Laflamme, N; Rivest, S;
Indirizzi:
CHU Laval, Ctr Rech, Mol Endocrinol Lab, Quebec City, PQ G1V 4G2, Canada CHU Laval Quebec City PQ Canada G1V 4G2 , Quebec City, PQ G1V 4G2, Canada Univ Laval, Dept Anat & Physiol, Quebec City, PQ G1V 4G2, Canada Univ Laval Quebec City PQ Canada G1V 4G2 Quebec City, PQ G1V 4G2, Canada
Titolo Testata:
JOURNAL OF COMPARATIVE NEUROLOGY
fascicolo: 4, volume: 434, anno: 2001,
pagine: 461 - 477
SICI:
0021-9967(20010611)434:4<461:ROTGET>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; INNATE IMMUNE-RESPONSE; CENTRAL-NERVOUS-SYSTEM; TUMOR-NECROSIS-FACTOR; ALPHA MESSENGER-RNA; TRANSCRIPTIONAL ACTIVATION; INHIBITORY FACTOR; CELLULAR-POPULATIONS; CHEMOKINE EXPRESSION; ONCOSTATIN-M;
Keywords:
circumventricular organs; endothelium; innate immune response; in situ hybridization histochemistry; inflammation; lipopolysaccharide; microglia; macrophages; NF-kappa B; septic shock;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Rivest, S CHU Laval, Ctr Rech, Mol Endocrinol Lab, 2705 Blvd Laurier, Quebec City, PQ G1V 4G2, Canada CHU Laval 2705 Blvd Laurier Quebec City PQ Canada G1V 4G2 Canada
Citazione:
I. Thibeault et al., "Regulation of the gene encoding the monocyte chemoattractant protein 1 (MCP-1) in the mouse and rat brain in response to circulating LPS and proinflammatory cytokines", J COMP NEUR, 434(4), 2001, pp. 461-477

Abstract

Accumulating evidence supports the existence of an innate immune response in the brain during systemic inflammation that is associated with a robust induction of proinflammatory cytokines and chemokines by specific cells of the central nervous system. The present study investigated the genetic regulation and fine cellular distribution of the monocyte chemoattractant protein-1 (MCP-1) in the brain of mice and rats in response to systemic immune insults. MCP-1 belongs to a superfamily of chemokines that have a leading sole in the early chemotaxic events during inflammation. In situ hybridization histochemistry failed to detect constitutive expression of the chemokine transcript in the cerebral tissue except for the area postrema (AP) that exhibited a low signal under basal conditions. This contrasts with the strongand transient induction of the mRNA encoding MCP-1 following a single systemic bolus of lipopolysaccharide (LPS), recombinant interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha). These stimuli rapidly triggered (30 to 90 minutes) MCP-1 transcription in all the circumventricular organs (CVOs), the choroid plexus (chp), the leptomeninges, and along the cerebral blood vessels. The time-related induction and intensity of the signal differed among the challenges, route of administration and species, but MCP-1-expressing cells were always found in vascular-associated structures and those devoid of blood-brain barrier. At later times, few isolated microglia across the brain parenchyma depicted positive signal for MCP-1 mRNA. A dual-labeling procedure also provided convincing anatomical evidence that endothelial cells of the microvasculature and a few myeloid cells of theCVOs and chp were positive for the transcript during endotoxemia. This gene is under a sophisticated transcriptional regulation, as the hybridizationsignal returned to undetectable levels 12 to 24 hours after all the treatments in both species. Of interest are the data that only ligands that triggered nuclear factor kappa 8 (NF-kappaB) signaling had the ability to increase MCP-1 gene expression, because high doses of IL-6 remained without effects. These data provide the anatomical evidence that MCP-1 is expressed within specific populations of cells in response to systemic inflammatory molecules that use NF-kappaB as intracellular signaling system. This chemokine may therefore play a critical role in the cerebral innate immune response and contribute to the early chemotaxic events during chronic cerebral inflammation. J. Comp. Neurol. 434:461-477, 2001. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:49:41