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Inflamm Bowel Dis. 2005 Oct;11(10):883-9.

DSS-induced colitis is exacerbated in STAT-6 knockout mice.

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Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, 71130, USA.



Several transcription factors have been proposed to regulate IBD including the signal transducer and activator of transcription-6 (STAT-6).


The role of STAT-6 was examined in the 5% dextran sulfate sodium (DSS)-induced murine model of colitis using STAT-6 and wildtype mice.


The disease activity index (DAI) revealed a significant increase in DAI in STAT-6 mice over STAT-6 mice given DSS. Both STAT-6 and wildtype mice displayed severe inflammation and crypt damage. Additionally, STAT-6 mice showed significant injury to the proximal colon compared with their littermate controls. Furthermore, STAT-6 mice receiving DSS had dramatically higher levels of serum nitrite/nitrate than all other groups. STAT-6 animals also displayed higher levels of inteferon-gamma than wildtype mice.


Because STAT-6 has been reported to regulate the expression and activity of inducible NO synthase (iNOS), our data suggest that, in DSS colitis, STAT-6 may modulate iNOS, to limit NO formation and control the extent of inflammation in the colon. We conclude that STAT-6 may normally play an important regulatory role in the pathogenesis of inflammatory bowel disease, possibly through modulation of iNOS and interferon-gamma.

[Indexed for MEDLINE]

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