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首页> 外文期刊>American Journal of Physiology >Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation.
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Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation.

机译：硫酸葡聚糖钠诱导的急性结肠炎在C57BL / 6中进展为慢性，但在BALB / c小鼠中则未发展为慢性：症状与炎症之间的相关性。

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摘要

Exposure to dextran sulfate sodium (DSS) induces acute colitis, which is normally resolved after DSS removal. To study chronicity, mice are typically subjected to three to five cycles of weekly DSS exposures, each followed by a 1- to 2-wk rest period. Here, we describe a novel and convenient way of inducing chronic, progressive colitis by a single exposure to DSS. C57BL/6 mice exposed to DSS for 5 days developed acute colitis that progressed to severe chronic inflammation. The plasma haptoglobin levels remained high during the chronic phase, showing that the inflammation was active. Surprisingly, the mice regained their original weight along with the progression of colitis, and the only apparent symptom was loose feces. Histopathological changes 4 wk after DSS removal were dense infiltrates of mononuclear cells, irregular epithelial structure, and persistent deposits of collagen. A progressive production of the cytokines IL-1beta, IL-12 p70, and IL-17 correlated with the extensive cellular infiltration, whereas high IFN-gamma production was mainly found late in the chronic phase. Similar to C57BL/6 mice, BALB/c mice exposed to 5 days of DSS developed acute colitis as previously described. The acute colitis was accompanied by elevated plasma levels of haptoglobin and increased colonic levels of IL-1alpha/beta, IL-6, IL-18, and granulocyte colony-stimulating factor. However, soon after DSS removal, BALB/c mice recovered and were symptom free within 2 wk and completely recovered 4 wk after DSS removal in terms of histopathology, haptoglobin levels, and local cytokine production. In summary, these data stress the effect of genetic background on the outcome of DSS provocation. We believe that the present protocol to induce chronic colitis in C57BL/6 mice offers a robust model for validating future therapies for treatment of inflammatory bowel disease.
机译：暴露于硫酸葡聚糖钠（DSS）会引起急性结肠炎，通常在去除DSS后即可解决。为了研究慢性病，通常每周对小鼠进行三到五个周期的DSS暴露，每个周期后休息1至2周。在这里，我们描述了通过单次暴露于DSS诱导慢性进行性结肠炎的新颖便捷的方法。暴露于DSS 5天的C57BL / 6小鼠发展为急性结肠炎，并发展为严重的慢性炎症。在慢性阶段血浆触珠蛋白水平保持较高，表明炎症活跃。出人意料的是，随着结肠炎的进展，小鼠恢复了原来的体重，唯一明显的症状是粪便稀疏。 DSS去除后4周的组织病理学变化是单核细胞浸润密集，上皮结构不规则以及胶原蛋白持续沉积。细胞因子IL-1β，IL-12 p70和IL-17的逐步产生与广泛的细胞浸润相关，而高IFN-γ产生主要在慢性期后期发现。类似于C57BL / 6小鼠，暴露于DSS 5天的BALB / c小鼠发生了急性结肠炎，如前所述。急性结肠炎伴有血浆触珠蛋白水平升高，IL-1α/β，IL-6，IL-18和粒细胞集落刺激因子的结肠水平升高。然而，在去除DSS后不久，BALB / c小鼠恢复了健康，并且在2周内无症状，在组织病理学，触珠蛋白水平和局部细胞因子产生方面，DSS去除后4 wk完全恢复。总之，这些数据强调了遗传背景对DSS激发结果的影响。我们认为，本发明的在C57BL / 6小鼠中诱导慢性结肠炎的方案为验证将来用于治疗炎性肠病的疗法提供了强有力的模型。

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