DSS-induced colitis is exacerbated in STAT-6 knockout mice
JW Elrod, SF Laroux, J Houghton… - Inflammatory bowel …, 2005 - academic.oup.com
JW Elrod, SF Laroux, J Houghton, A Carpenter, T Ando, MH Jennings, M Grisham, N Walker…
Inflammatory bowel diseases, 2005•academic.oup.comBackground 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 …
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 …
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-γ 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-γ.
Oxford University Press