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首页> 外文期刊>Journal of Cellular Physiology >Exacerbated tissue destruction in DSS-induced acute colitis of OPN-null mice is associated with downregulation of TNF-alpha expression and non-programmed cell death.
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Exacerbated tissue destruction in DSS-induced acute colitis of OPN-null mice is associated with downregulation of TNF-alpha expression and non-programmed cell death.

机译：在DSS-induced加剧了组织破坏与急性结肠炎OPN-null老鼠downregulation tnf的表达非程序细胞死亡。

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摘要

Osteopontin (OPN), a pro-inflammatory mediator, is constitutively expressed in normal gut and is upregulated in inflammatory colitis. To determine the significance of OPN in inflammatory bowel disease, we studied the development of acute, experimental colitis induced by dextran sulfate sodium (DSS) in OPN-null and wild-type (WT) mice. OPN expression was markedly increased in WT diseased colons, while a higher disease activity index, including spleen enlargement, bowel shortening, and mucosal destruction, was observed in OPN-null mice. Although peripheral blood neutrophil numbers were lower in DSS-treated OPN-null mice, tissue myeloperoxidase levels, reflecting enhanced neutrophil activity, were increased in the diseased colons. In comparison, lymphocyte numbers in peripheral blood were increased earlier than in DSS-treated WT mice. Despite a significantly greater spleen enlargement, flow cytometric analysis of splenocytes from the DSS-treated OPN-null mice revealed lower numbers of differentiated macrophages and (CD4+ and CD8alpha+) lymphocytes. Whereas pro-inflammatory cytokines, including G-CSF, RANTES, MIP1alpha, and TNF-alpha, were increased < 10-fold in DSS-treated WT splenocytes, expression of these cytokines was dramatically suppressed in the DSS-treated OPN-null splenocytes as well as gut tissues. The suppressed TNF-alpha response in OPN-null mice was reflected in a marked increase in non-apoptotic cell death in diseased colons. Collectively, these studies demonstrate that OPN is required for mucosal protection in acute inflammatory colitis.
机译：骨桥蛋白(OPN)、促炎症介质正常的肠道和是既定的调节炎症性结肠炎。在炎症性肠OPN的意义急性疾病,我们研究了发展,葡聚糖硫酸酯引起的实验性结肠炎钠(DSS) OPN-null和野生型小鼠(WT)。在WT OPN表达明显增加患病的冒号,而更高的疾病活动指数,包括脾肿大、肠缩短,黏膜破坏,被观察到在OPN-null老鼠。中性粒细胞数量在DSS-treated低OPN-null老鼠,组织髓过氧化物酶水平,反射增强中性粒细胞的活动,增加患病的冒号。在外周血淋巴细胞数量增加早于DSS-treated WT老鼠。尽管大大增强脾脏扩大,流动仪的分析脾细胞从DSS-treated OPN-null老鼠显示较低数量的分化巨噬细胞和淋巴细胞(CD4 +和CD8alpha +)。而促炎细胞因子,包括咆哮,g - csf MIP1alpha, tnf< 10倍增加DSS-treated WT脾细胞,这些细胞因子的表达DSS-treated显著抑制OPN-null脾细胞以及肠道组织。抑制tnf反应OPN-null老鼠反映在显著增加non-apoptotic细胞死亡在患病的冒号。总的来说,这些研究表明OPN需要在急性粘膜保护吗炎症性结肠炎。

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