| First Author | Erdman S | Year | 2001 |
| Journal | J Immunol | Volume | 166 |
| Issue | 3 | Pages | 1443-7 |
| PubMed ID | 11160181 | Mgi Jnum | J:67107 |
| Mgi Id | MGI:1929849 | Doi | 10.4049/jimmunol.166.3.1443 |
| Citation | Erdman S, et al. (2001) Typhlocolitis in NF-kappa B-deficient mice. J Immunol 166(3):1443-7 |
| abstractText | Activation of inflammatory gene expression by the transcription factor NF-kappaB is a central pathway in many inflammatory disorders, including colitis. Increased NF-kappaB activity has been linked with development of colitis in humans and animal models, thus it was unexpected when NF-kappaB-deficient mice developed spontaneous typhlocolitis. To further characterize this finding, we induced typhlocolitis in rederived NF-kappaB-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-kappaB and were also heterozygous for the p65 subunit of NF-kappaB(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-kappaB-deficient mice was normal. These data indicate that p50 and p65 subunits of NF-kappaB have an unexpected role in inhibiting the development of colitis. |
