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Typhlocolitis in NF-kappa B-deficient mice.
S Erdman1, J G Fox, C A Dangler
1Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. serdman@mit.edu
Journal of Immunology (Baltimore, Md. : 1950)
|February 13, 2001
Summary
Mice lacking key NF-kappaB subunits unexpectedly developed severe colitis. This suggests NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) plays a surprising role in preventing colitis development.
Area of Science:
- Immunology
- Molecular Biology
- Gastroenterology
Background:
- Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) is central to inflammatory gene expression.
- NF-kappaB activation is linked to colitis development in humans and animal models.
Purpose of the Study:
- To investigate the unexpected development of spontaneous typhlocolitis in NF-kappaB-deficient mice.
- To characterize the role of NF-kappaB subunits in Helicobacter hepaticus-induced colitis.
Main Methods:
- Induction of typhlocolitis in rederived NF-kappaB-deficient mice via intragastric Helicobacter hepaticus infection.
- Assessment of colitis severity and type 1 cytokine expression at 6 weeks postinfection.
- Analysis of T cell development in NF-kappaB-deficient mice.
Main Results:
- Mice lacking both p50 and p65 NF-kappaB subunits (p50(-/-)p65(+/-)) developed severe colitis with increased type 1 cytokine expression.
- Mice lacking only the p50 subunit (p50(-/-)) showed less severe colitis.
- Wild-type and p65(+/-) mice remained unaffected; T cell development was normal in deficient mice.
Conclusions:
- The p50 and p65 subunits of NF-kappaB unexpectedly inhibit the development of colitis.
- These findings challenge the established role of NF-kappaB in inflammatory disorders.