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Titolo:
NEUTROPHIL INFILTRATION, GLIAL REACTION, AND NEUROLOGICAL DISEASE IN TRANSGENIC MICE EXPRESSING THE CHEMOKINE N51 KC IN OLIGODENDROCYTES/
Autore:
TANI M; FUENTES ME; PETERSON JW; TRAPP BD; DURHAM SK; LOY JK; BRAVO R; RANSOHOFF RM; LIRA SA;
Indirizzi:
BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT ONCOL PRINCETON NJ 08543 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT ONCOL PRINCETON NJ 08543 BRISTOL MYERS SQUIBB PHARMACEUT RES INST,DEPT EXPTL PATHOL PRINCETON NJ 08543 CLEVELAND CLIN FDN,DEPT NEUROSCI,RES INST CLEVELAND OH 44195
Titolo Testata:
The Journal of clinical investigation
fascicolo: 2, volume: 98, anno: 1996,
pagine: 529 - 539
SICI:
0021-9738(1996)98:2<529:NIGRAN>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; BLOOD-BRAIN-BARRIER; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA; MONOCYTE CHEMOATTRACTANT PROTEIN-1; INTERCRINE CYTOKINE FAMILY; MOLECULAR-BIOLOGY; GROWTH-FACTOR; CEREBRAL-ISCHEMIA; CC-CHEMOKINES;
Keywords:
CHEMOTACTIC FACTORS; TRANSGENIC MICE; CYTOKINES; CENTRAL NERVOUS SYSTEM DISEASES; LEUKOCYTE TRAFFICKING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
74
Recensione:
Indirizzi per estratti:
Citazione:
M. Tani et al., "NEUTROPHIL INFILTRATION, GLIAL REACTION, AND NEUROLOGICAL DISEASE IN TRANSGENIC MICE EXPRESSING THE CHEMOKINE N51 KC IN OLIGODENDROCYTES/", The Journal of clinical investigation, 98(2), 1996, pp. 529-539

Abstract

Chemokines (pro-inflammatory chemoattractant cytokines) are expressedin pathological conditions of the central nervous system (CNS). Previous studies suggested that the CNS is relatively resistant to leukocyte diapedesis after chemokine injection, leaving their functional role unresolved. The CNS function of N51/KC, a neutrophil-selective chemokine, was addressed by expressing N51/KC under control of the myelin basic protein (MBP) promoter in transgenic (tg) mice (MBP-N51/KC mice). CNS-specific N51/KC expression produced remarkable neutrophil infiltration into perivascular, meningeal, and parenchymal sites, demonstratingthat this chemokine exerts the multiple functions in vivo required torecruit leukocytes into the CNS. MBP-N51/KC mice represent an incisive model for the molecular dissection of neutrophil entry into the CNS. Unexpectedly, MBP-N51/KC mice developed a neurological syndrome of pronounced postural instability and rigidity at high frequency beginningat 40 days of age, well after peak chemokine expression. 68/182 mice in one tg line were found dead before one year of age, with prominent neurological symptoms premortem in 26 (38%). Florid microglial activation and blood-brain barrier disruption without dysmyelination were themajor neuropathological alterations. Late-onset neurological symptomsin MBP-N51/KC mice may indicate unanticipated consequences of CNS chemokine expression.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 17/01/21 alle ore 18:14:50