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Titolo:
Genetic analysis of susceptibility to dextran sulfate sodium-induced colitis in mice
Autore:
Mahler, M; Bristol, IJ; Sundberg, JP; Churchill, GA; Birkenmeier, EH; Elson, CO; Leiter, EH;
Indirizzi:
Jackson Lab, Bar Harbor, ME 04609 USA Jackson Lab Bar Harbor ME USA 04609Jackson Lab, Bar Harbor, ME 04609 USA Cornell Univ, Dept Biostat, Ithaca, NY 14853 USA Cornell Univ Ithaca NY USA 14853 Univ, Dept Biostat, Ithaca, NY 14853 USA Univ Alabama, Dept Med, Birmingham, AL 35294 USA Univ Alabama Birmingham AL USA 35294 , Dept Med, Birmingham, AL 35294 USA
Titolo Testata:
GENOMICS
fascicolo: 2, volume: 55, anno: 1999,
pagine: 147 - 156
SICI:
0888-7543(19990115)55:2<147:GAOSTD>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
INFLAMMATORY BOWEL-DISEASE; CHRONIC ULCERATIVE-COLITIS; CD4(+) T-CELLS; CROHNS-DISEASE; INTESTINAL INFLAMMATION; IMMUNODEFICIENT MICE; AUTOIMMUNE-DISEASE; CONGENIC STRAINS; NOD MICE; MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Leiter, EH Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA Jackson Lab 600 Main St Bar Harbor ME USA 04609 r, ME 04609 USA
Citazione:
M. Mahler et al., "Genetic analysis of susceptibility to dextran sulfate sodium-induced colitis in mice", GENOMICS, 55(2), 1999, pp. 147-156

Abstract

The genetic basis for differential sensitivity of inbred mice to inflammatory bowel disease induced by dextran sulfate sodium (DSS) is unknown. Susceptible C3H/ReJ were outcrossed to partially resistant C57BL/6J mice. F2 andN2 progeny were phenotyped by evaluating histopathologic lesions in large intestine detected 16 days after a 5-day period of feeding 3.5% DSS. Screening for DSS colitis (Dssc) loci revealed quantitative trait loci (QTL) on Chr 5 (Dssc1) and Chr 2 (Dssc2). These traits contributed additively, explaining 17.5% of the variation in total colonic lesions. Additional QTL on Chr18 and 1 that collectively explained 11% of the variation in total colon lesions were indicated. In the cecum, only a putative QTL on Chr 11 was associated with pathology (lesion severity) in the cecum. Reduced DSS susceptibility was observed in congenic stocks in which the highly susceptible NOD/Lt strain carried putative resistance alleles from either B6 on Chr 2 or from the highly resistant NON/Lt strain on Chr 9. We conclude that multiple genes control susceptibility to DSS colitis in mice. Possible Dssc candidate genes are discussed in terms of current knowledge of inflammatory bowel disease susceptibility loci in humans. (C) 1999 Academic Press.

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Documento generato il 02/04/20 alle ore 21:20:16