Cutting edge:: Typhlocolitis in NF-κB-deficient mice
Cutting edge:: Typhlocolitis in NF-κB-deficient mice
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DOI：
10.4049/jimmunol.166.3.1443
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发表时间：
2001-02-01
影响因子：
4.4
通讯作者：
Horwitz, BH
中科院分区：
文献类型：
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作者：
Erdman, SE;Fox, JG;Horwitz, BH
转录因子NF-κ B激活炎性基因表达是许多炎性疾病（包括结肠炎）的中心途径。在人类和动物模型中，增加的NF-κ B活性与结肠炎的发生有关，因此当NF-κ B缺陷小鼠发生自发性结肠炎时是出乎意料的。为了进一步描述这一发现，我们用肝螺杆菌胃内感染再衍生的NF-κ B缺陷小鼠，诱导结肠炎。在感染后6周（PI），在缺乏NF-κ B p50亚基且NF-κ B p65亚基杂合（p50（-/-）p65（+/-））的感染小鼠中观察到严重的结肠炎伴1型细胞因子表达增加。单独缺乏p50亚基（p50（-/-））的小鼠受影响不太严重，野生型小鼠和p65（+/-）小鼠不受影响。NF-κ B缺陷小鼠的T细胞发育正常。这些数据表明NF-κ B的p50和p65亚基在抑制结肠炎的发展中具有意想不到的作用。
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.