Format

Send to

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

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

Author information

1
Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, 71130, USA.

Abstract

BACKGROUND:

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

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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]

Supplemental Content

Loading ...
Support Center