Expression data of lamina propria macrophages from LysMCre and LysMCre;Arntfl/fl mice with DSS-induced acute colitis

Mice with myeloid ARNT deficiency (LysMCre;Arntfl/fl mice) exhibit defective resolution of DSS-induced acute colitis compared to LysMCre mice. This microarray is carried out to compare the phenotype of lamina propria macrophages from the two cohorts, and to identify factors that are disrupted by myeloid ARNT deficiency and can potentially contribute to the defective resolution of acute colitis. LysMCre mice were used as control animals with intact Arnt alleles in myeloid populations. LysMCre;Arntfl/fl mice were the experimental animals with conditionally deleted Arnt in myeloid cells. Five female LysMCre mice and four female LysMCre;Arntfl/fl mice were co-housed and subjected to DSS-induced colitis (3% dextran sodium sulfate (DSS) in drinking water for 5 days, followed by 3 days on regular drinking water). Lamina propria macrophages (CD45+, CD11b+, F4/80+) were isolated by flow sorting on Day 8.

与溶菌酶M-Cre（LysMCre）小鼠相比，髓系ARNT缺陷型小鼠（LysMCre;Arntfl/fl小鼠）存在葡聚糖硫酸钠（Dextran Sodium Sulfate, DSS）诱导的急性结肠炎消退缺陷。本基因芯片（microarray）实验旨在比较两组小鼠的固有层巨噬细胞表型，并鉴定受髓系ARNT缺陷干扰、且可能参与急性结肠炎消退缺陷的潜在调控因子。其中，LysMCre小鼠作为对照组，其髓系细胞内的Arnt等位基因完整；LysMCre;Arntfl/fl小鼠为实验组，其髓系细胞中的Arnt基因被条件性敲除。实验中，将5只雌性LysMCre小鼠与4只雌性LysMCre;Arntfl/fl小鼠同笼饲养，随后以3%葡聚糖硫酸钠饮水饲喂5天，再更换为正常饮水饲喂3天，以此构建DSS诱导的结肠炎模型。于造模第8天，通过流式分选分离得到固有层巨噬细胞（CD45+、CD11b+、F4/80+）。