Impaired deoxyribonuclease I activity in patients with inflammatory bowel diseases.
Impaired deoxyribonuclease I activity in patients with inflammatory bowel diseases.
复制标题
DOI：
10.4061/2011/945861
复制
发表时间：
2011
影响因子：
4
通讯作者：
Lukáš M
中科院分区：
文献类型：
--
作者：
Malíčková K;Duricová D;Bortlík M;Hrušková Z;Svobodová B;Machková N;Komárek V;Fučíková T;Janatková I;Zima T;Lukáš M
背景和目标。脱氧核糖核酸酶I（DNaseI）是一种内切核酸酶，其促进染色质分解并促进对自身免疫性疾病的易感性。本研究旨在探讨炎症性肠病（IBD）患者血清DNA酶I活性。患者和方法。对110例IBD患者的队列进行了评价，年龄为35 ± 12岁，其中77例患有克罗恩病（CD），33例患有溃疡性结肠炎（UC）。选择50例SLE患者和50例健康献血员作为对照组。 结果IBD患者的DNase I活性显著低于健康人，但高于SLE患者（P <0.0001）。UC患者的DNase I活性高于CD患者，P = 0.21。女性IBD患者的DNA酶I活性显著低于男性，P = 0.024;然而，在健康个体中，DNA酶I活性与性别无关。 DNA酶I活性与自身免疫性（SLE + IBD）队列以及单独IBD队列中的抗核小体抗体血清浓度呈强负相关。 结论.血清DNA酶I活性降低可能具有IBD的发病后果。 针对核小体的自身抗体的诱导可能是受损的DNA酶I活性的反映。
Background and Aims. Deoxyribonuclease I (DNaseI) is an endonuclease that facilitates chromatin breakdown and promotes susceptibility to autoimmune disorders. The aim of current study was to investigate serum DNase I activity in patients with inflammatory bowel diseases (IBD). Patients and Methods. A cohort of 110 IBD patients was evaluated, aged 35 ± 12 years, 77 with Crohn's disease (CD) and 33 with ulcerative colitis (UC). 50 SLE patients and 50 healthy blood donors were examined as control groups. Results. DNase I activity in IBD patients was significantly lower than in healthy individuals, but higher than in SLE patients (P < .0001). Patients with UC showed higher DNase I activity than CD patients, P = .21. DNase I activity in female patients with IBD was significantly lower than in males, P = .024; however, no differences in DNase I activity were found in relation to gender in healthy individuals. DNase I activity has shown a strong negative correlation with the serum concentration of anti-nucleosomal antibodies in the autoimmune (SLE + IBD) cohort, as well as in the separate IBD cohort. Conclusions. Reduced serum DNase I activity probably has pathogenetic consequences in IBD. Induction of autoantibodies towards nucleosomes could be a reflection of impaired DNase I activity.