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Titolo:
INDUCTION OF MACROPHAGE INFLAMMATORY PROTEIN-2 GENE-EXPRESSION BY INTERLEUKIN-1-BETA IN RAT LUNG
Autore:
XU WB; HADDAD EB; TSUKAGOSHI H; ADCOCK I; BARNES PJ; CHUNG KF;
Indirizzi:
NATL HEART & LUNG INST,DEPT THORAC MED,DOVEHOUSE ST LONDON SW3 6LY ENGLAND NATL HEART & LUNG INST,DEPT THORAC MED LONDON SW3 6LY ENGLAND
Titolo Testata:
Thorax
fascicolo: 11, volume: 50, anno: 1995,
pagine: 1136 - 1140
SICI:
0040-6376(1995)50:11<1136:IOMIPG>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALVEOLAR MACROPHAGES; EPITHELIAL-CELLS; MESSENGER-RNA; RELEASE; CYTOKINES; FAMILY;
Keywords:
INTERLEUKIN 1-BETA; MACROPHAGE INFLAMMATORY PROTEIN 2 (MIP-2); CHEMOKINES; NEUTROPHIL; LUNG INFLAMMATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
W.B. Xu et al., "INDUCTION OF MACROPHAGE INFLAMMATORY PROTEIN-2 GENE-EXPRESSION BY INTERLEUKIN-1-BETA IN RAT LUNG", Thorax, 50(11), 1995, pp. 1136-1140

Abstract

Background - Recruitment of inflammatory cells in the lungs may contribute to tissue injury as a result of mediators released from these cells. Interleukin 1 beta (IL-1 beta) is a potent;inducer of neutrophil accumulation, a process that may require local protein biosynthesis. Macrophage inflammatory protein 2 (MIP-2) is a similar to 6 kD heparin binding protein and is a member of the C-X-C superfamily that causes significant neutrophil chemotaxis and activation in vitro. A study was performed to determine whether IL-1 beta could induce the expression of MIP-2 in the lungs of Brown-Norway rats. Methods - rhIL-1 beta (500 U) or 0.9% NaCl was injected intratracheally and bronchoalveolar lavage (BAL) cells and lung tissues were evaluated for MIP-2 mRNA expression after RNA extraction by Northern blot analysis. MIP-2 probe was prepared from cDNA obtained by reverse transcriptase-polymerase chain reaction (RT-PCR) of BAL cells obtained from a rat treated with lipopolysaccharide. Results - There was no detectable MIP-2 mRNA in the lungs ofcontrol rats but a marked enhancement of the expression at four hourswith no expression at 12 hours and a slight expression at 24 hours. IL-1 beta induced a significant influx of neutrophils into BAL fluid with a transient increase in macrophages, In situ hybridisation of lungsusing MIP-2 cDNA probe labelled with digoxigenin showed expression ofMIP-2 mRNA in ah-way mononuclear cells and airway epithelium at four hours after IL-1 beta; at 24 hours the signal had nearly gone. Conclusion - IL-1 beta induces the expression of MIP-2 mRNA in rat lung. MIP-2 may be one chemokine that could contribute to IL-1 beta induced neutrophil influx.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 00:47:28