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Titolo:
A NOVEL MODEL OF INFLAMMATORY BOWEL-DISEASE - MICE DEFICIENT FOR THE MULTIPLE-DRUG RESISTANCE GENE, MDR1A, SPONTANEOUSLY DEVELOP COLITIS
Autore:
PANWALA CM; JONES JC; VINEY JL;
Indirizzi:
IMMUNEX RES & DEV CORP,DEPT MOL IMMUNOL,51 UNIV ST SEATTLE WA 98101 IMMUNEX RES & DEV CORP,DEPT MOL IMMUNOL SEATTLE WA 98101 IMMUNEX RES & DEV CORP,DEPT IMMUNOBIOL SEATTLE WA 98101
Titolo Testata:
The Journal of immunology (1950)
fascicolo: 10, volume: 161, anno: 1998,
pagine: 5733 - 5744
SICI:
0022-1767(1998)161:10<5733:ANMOIB>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC INTESTINAL INFLAMMATION; BLOOD-BRAIN-BARRIER; P-GLYCOPROTEIN; T-CELLS; MULTIDRUG-RESISTANCE; SCID MICE; ULCERATIVE-COLITIS; BACTERIAL-FLORA; WASTING DISEASE; LAMINA PROPRIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
51
Recensione:
Indirizzi per estratti:
Citazione:
C.M. Panwala et al., "A NOVEL MODEL OF INFLAMMATORY BOWEL-DISEASE - MICE DEFICIENT FOR THE MULTIPLE-DRUG RESISTANCE GENE, MDR1A, SPONTANEOUSLY DEVELOP COLITIS", The Journal of immunology (1950), 161(10), 1998, pp. 5733-5744

Abstract

The murine multiple drug resistance (mdr) gene, mdr1a, encodes a 170-kDa transmembrane protein that is expressed in many tissues including intestinal epithelial cells, a subset of lymphoid cells and hematopoietic cells. We report that mdr-Ia knockout (mdr1a(-/-)) mice are susceptible to developing a severe, spontaneous intestinal inflammation whenmaintained under specific pathogen-free animal facility conditions. The intestinal inflammation seen in mdr1a(-/-) mice has a pathology similar to that of human inflammatory bowel disease (IBD) and is defined by dysregulated epithelial cell growth and leukocytic infiltration into the lamina propria of the large intestine. Treating mdr1a(-/-) mice with oral antibiotics can both prevent the development of disease and resolve active inflammation. Lymphoid cells isolated from mice with active colitis are functionally reactive to intestinal bacterial Ags, providing evidence that there is enhanced immunologic responsiveness to the normal bacterial flora during IBD. This study is the first description of spontaneous colitis in a gene knockout mouse with an apparently intact immune system. This novel model of spontaneous colitis may provide new insight into the pathogenesis of IBD, the nature of dysregulated immune reactivity to intestinal bacterial Ags, and the potential functional role of mdr genes expressed in the cells and tissues of thecolonic microenvironment.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 00:57:52