Transcriptome profiling of gene expression in the colon tissues of steady state and Helicobacter hepaticus-infected 129SvEvS6.Rag2-/- mice and the congenic strain 129.C3B.Rag2-/- R17

Chronic inflammation of the intestine has been associated with an elevated risk of developing colorectal cancer. Recent association studies have highlighted the role of genetic predisposition in the etiology of colitis and started to unravel its complexity. However, the genetic factors influencing the progression from colon inflammation to tumorigenesis are not known. We used Helicobacter hepaticus-induced colitis in a 129.RAG(-/-) mouse model to explore early onset of the disease. Experiments purpose and justifications: to elucidate early genes and pathways changed in the mouse strain susceptible to innate colitis triggered by Hh infection. Experimental factors: steady state, and days 2 and 4 of infection (n=4 mice per condition). The time course is validated on the same samples using qPCR for inflammatory genes. Samples: RNA from proximal mouse colon. Two mouse genetic strains are compared 129Rag-/- (susceptible) and 129.R17Rag-/- (protected from colitis).肠道慢性炎症与结直肠癌发病风险升高存在显著关联。近期的关联研究已阐明遗传易感性在结肠炎病因学中的作用，并开始揭示其发病机制的复杂性。然而，调控结肠炎症向肿瘤发生进展的遗传因子仍未明确。本研究借助129.RAG(-/-)小鼠模型中肝螺杆菌（Helicobacter hepaticus）诱导的结肠炎，探究该疾病的早期发病进程。实验目的与依据为：阐明经Hh感染诱发的先天性结肠炎易感小鼠品系中发生表达改变的早期基因及信号通路。实验处理因素包括：稳态对照组，以及感染后第2天、第4天的样本（每组设置4只小鼠）。该时间进程已通过针对炎症基因的qPCR实验在相同样本中得到验证。样本取自小鼠近端结肠的RNA。本研究比较了两种小鼠遗传品系：129Rag-/-（结肠炎易感型）与129.R17Rag-/-（结肠炎抵抗型）。