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Titolo:
TNF-ALPHA-MEDIATED EXPRESSION OF THE RECEPTOR FOR ANAPHYLATOXIN-C5A ON NEURONS IN EXPERIMENTAL LISTERIA MENINGOENCEPHALITIS
Autore:
STAHEL PF; FREI K; EUGSTER HP; FONTANA A; HUMMEL KM; WETSEL RA; AMES RS; BARNUM SR;
Indirizzi:
UNIV ALABAMA,DEPT MICROBIOL,DIV CLIN IMMUNOL & RHEUMATOL,BHS 306,1918UNIV BLVD BIRMINGHAM AL 35294 UNIV ALABAMA,DEPT MICROBIOL,DIV CLIN IMMUNOL & RHEUMATOL BIRMINGHAM AL 35294 UNIV ALABAMA,DEPT MED,DIV CLIN IMMUNOL & RHEUMATOL BIRMINGHAM AL 35294 UNIV ZURICH HOSP,DEPT INTERNAL MED,CLIN IMMUNOL SECT ZURICH SWITZERLAND UNIV ALABAMA,DEPT NEUROSURG BIRMINGHAM AL 35294 UNIV TEXAS,HLTH SCI CTR,INST MOL MED HOUSTON TX 77030 SMITHKLINE BEECHAM PHARMACEUT,DEPT MOL IMMUNOL KING OF PRUSSIA PA 19406
Titolo Testata:
The Journal of immunology
fascicolo: 2, volume: 159, anno: 1997,
pagine: 861 - 869
SICI:
0022-1767(1997)159:2<861:TEOTRF>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; CENTRAL-NERVOUS-SYSTEM; BACTERIAL-MENINGITIS; CEREBROSPINAL-FLUID; MONOCLONAL-ANTIBODIES; POLYMORPHONUCLEAR LEUKOCYTES; PNEUMOCOCCAL MENINGITIS; MENINGEAL INFLAMMATION; INFECTIOUS MENINGITIS; CHEMOTACTIC ACTIVITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
60
Recensione:
Indirizzi per estratti:
Citazione:
P.F. Stahel et al., "TNF-ALPHA-MEDIATED EXPRESSION OF THE RECEPTOR FOR ANAPHYLATOXIN-C5A ON NEURONS IN EXPERIMENTAL LISTERIA MENINGOENCEPHALITIS", The Journal of immunology, 159(2), 1997, pp. 861-869

Abstract

The anaphylatoxin C5a has been implicated in the pathogenesis of bacterial meningitis as a potent mediator of inflammation in the subarachnoid space. We investigated the expression of the receptor for C5a (C5aR) in brains of mice with experimental Listeria monocytogenes (LM) meningoencephatitis. In the course of the disease, infiltrating cells in the meninges and the ventricles were found to express C5aR mRNA and protein. In the brain parenchyma, very low constitutive C5aR expression was seen on pyramidal neurons and Purkinje cells. However, in LM-infected mice, a dramatic increase in C5aR expression occurred on neurons starting 6 h after infection and was maximal between 24 and 36 h. TNF-alpha was identified as an essential mediator of neuronal C5aR expression, since mice lacking the genes for TNF and Iymphotoxin-alpha (TNF/lymphotoxin-alpha -/- mice) showed significantly attenuated C5aR expression after LM infection. Furthermore, i.p. injection of recombinant TNF-alpha induced enhanced C5aR expression in the brains of TNF/lymphotoxin-alpha -/- mice and in normal animals even in the absence of a bacterial infection. We also assessed the levels of anaphylatoxin C5a in the cerebrospinal fluid of patients with infectious meningitis. C5a was detected in all patients with bacterial meningitis (n = 9), in 6 of 18patients with aseptic meningitis, and in 1 of 66 control patients. The finding of TNF-alpha-mediated C5aR expression on neurons in experimental Listeria meningitis and the detection of the ligand, C5a, in the cerebrospinal fluid of human patients with infectious meningitis present new directions in the investigation of the pathophysiologic sequelae leading to secondary brain damage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/01/21 alle ore 00:51:35