Background: The presence of neutrophil-rich inflammation in colon tissues of patients with ulcerative colitis (UC) is one of the most important histological characteristics of this disease. However, the expression of CXCL chemokines governing the infiltration of neutrophils in UC has not been well elucidated.
Materials and methods: In this experimental study, the UC model was induced in Wistar rats by administration of 2 mL 4% acetic acid into the large colon through the rectum. Animals were anesthetized after 48 hrs; their colon tissue samples were isolated for macroscopic and histopathological examinations. The expression of CXCL family was assessed by reverse transcription polymerase chain reaction (qRT-PCR) technique.
Results: Heavy infiltration of neutrophils, coagulation necrosis, and ulcers were observed in H&E staining, which pathologically proved the UC model. qRT-PCR results showed that ELR^+, CXC chemokines such as CXCL6 and CXCL3 had the highest expression in the UC group, which was 49 and 28 times higher than that of the control group, respectively. In addition, other chemokines of this group including CXCL1, CXCL2, and CXCL7 had a significant increase compared to the control group (P≤0.05). However, ELR^−, CXC chemokines such as CXCL4, CXCL13, and CXCL16 showed a smaller upregulation, while CXCL14 chemokine showed a significant decrease compared to the control group (P≤0.05). However, the expression of CXCL9-12 and CXCL17 did not change.
Conclusion: The results showed that the ELR^+, CXC chemokines, especially CXCL6 and CXCL3, many involved in the pathogenesis of UC; therefore, CXCL6 and CXCL3 chemokines can be used as therapeutic targets for UC, although more studies using human samples are required.



中文翻译：

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ELR阳性CXCL趋化因子在溃疡性结肠炎的动物模型中高度表达。

背景：溃疡性结肠炎（UC）患者结肠组织中富含嗜中性白细胞的炎症是该疾病最重要的组织学特征之一。但是，尚未很好地阐明控制UC中性粒细胞浸润的CXCL趋化因子的表达。
材料和方法：在本实验研究中，通过向直肠大肠内注入2 mL 4％乙酸，在Wistar大鼠中诱发UC模型。48小时后将动物麻醉。分离出它们的结肠组织样品以进行宏观和组织病理学检查。通过逆转录聚合酶链反应（qRT-PCR）技术评估CXCL家族的表达。
结果：在H＆E染色中观察到嗜中性粒细胞大量浸润，凝血坏死和溃疡，这在病理上证明了UC模型。qRT-PCR结果表明，UCR组中ELR ^+， CXC趋化因子如CXCL6和CXCL3的表达最高，分别比对照组高49倍和28倍。此外，与对照组相比，该组的其他趋化因子包括CXCL1，CXCL2和CXCL7均有显着增加（P≤0.05）。但是，与对照组相比，ELR- ^， CXC趋化因子如CXCL4，CXCL13和CXCL16表现出较小的上调，而CXCL14趋化因子表现出明显的降低（P≤0.05）。但是，CXCL9-12和CXCL17的表达没有改变。
结论：结果表明，ELR ^+， CXC趋化因子特别是CXCL6和CXCL3参与了UC的发病机制。因此，CXCL6和CXCL3趋化因子可以用作UC的治疗靶标，尽管需要使用人体样品进行更多的研究。