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CUTTING EDGE |
B-Deficient Mice1
,
*
Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139;
Department of Pathology, Immunology Research Division, Brigham and Women’s Hospital, Boston, MA 02115; and
Division of Emergency Medicine, Children’s Hospital, Boston, MA 02115
Activation of inflammatory gene expression by the transcription
factor NF-
B is a central pathway in many inflammatory disorders,
including colitis. Increased NF-B activity has been linked with
development of colitis in humans and animal models, thus it was
unexpected when NF-B-deficient mice developed spontaneous
typhlocolitis. To further characterize this finding, we induced
typhlocolitis in rederived NF-B-deficient mice using intragastric
infection with Helicobacter hepaticus. At 6 wk
postinfection (PI), severe colitis with increased type 1 cytokine
expression was seen in infected mice that lacked the p50 subunit of
NF-B and were also heterozygous for the p65 subunit of
NF-B(p50-/-p65+/-). Mice lacking the p50
subunit alone (p50-/-) were less severely affected, and
wild-type mice and p65+/- mice were unaffected. T cell
development in NF-B-deficient mice was normal. These data indicate
that p50 and p65 subunits of NF-B have an unexpected role in
inhibiting the development of colitis.
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