溃疡性结肠炎患者外周血中性粒细胞凋亡与CRP、IL-6水平的关系

目的 观察溃疡性结肠炎(UC)患者外周血中性粒细胞(PMN)凋亡的变化，并检测C反应蛋白(CRLP)、IL-6水平的变化，探讨UC患者PMN凋亡与CRP、IL-6水平的关系。方法 采用流式细胞术检测28例UC病人外周血PMN凋亡。结果 活动期UC患者PMN凋亡率明显低于健康人对照组和缓解期UC患者。缓解期UC患者PMN凋亡率与对照组无差别。不同病情活动期UC患者PMN凋亡有显著性差异。活动期UC患者外周血中CRP、IL-6水平均高于对照组和缓解组，且与PMN凋亡呈负相关，与病情呈正相关。缓解组患者CRP、IL-6与对照组无显著性差异。结论 UC患者PMN凋亡延迟，且与病情及疗效密切相关。IL-6产生过多可导致肝脏合成CRP增高，同时可能是导致PMN凋亡延迟的重要因素。适度调控PMN凋亡。有可能会成为治疗UC的有效途径。

Relationship between apoptosis of neutrophil and expression of C reactive protein and IL-6 in patients with ulcerative colitis

To observe the changes of neutrophil (PMN) apoptosis and the levels of C reactive protein and IL-6 in patients with ulcerative colitis (UC) and to study the relationship between them. The apoptosis of neutrophil in 28 patients with UC at the active stage and 13 patients with UC at the remission stage were determined with flow cytometry, CRP and IL-6 were determined with rate nephelometry and ELISA method respectively. The percentage of neutrophil apoptosis in the patients with UC at the active stage was obviously lower than that of healthy persons and the patients with UC at the remission stage. There were no differential significance of neutrophil apoptosis between healthy persons and patients with UC at remission stage. Significant differences in apoptosis of neutrophil were found among the different clinical stages of active UC patients. The levels of CRP and in patients with UC at the active stage were higher than that of healthy persons and the patients with UC at the remission stage significantly, and the increasing levels of CRP and IL-6 in active UC patients were negatively correlated to the percentage of neutrophil apoptosis and positively correlated to the severity of UC. [Conclusion] The data demonstrated a delay in apoptotic process of neutrophil in active UC. The high expression of IL-6 could stimulate the synthesis of CRP by liver cell, and may play an important role in the cause of inhibition of neutrophil apoptosis which prolong the functional life span of neutrophil. Therefor, the delayed apoptotic neutrophils produce more inflammatory mediators participating in the damage of colonic tissue. For this reason, adjusting the expression of cytokines and moderately controlling the apoptosis of neutrophil further may be a new therapeutic target for UC.