Kotłowska-Kmieć Aldona, Bakowska Alicja, Wołowska Ewa, Łuczak Grazyna, Liberek Anna
Specjalistyczny ZOZ Nad Matka i Dzieckiem w Gdańsku, Oddział Interny Dzieci, 80-308 Gdańsk.
Med Wieku Rozwoj. 2009 Oct-Dec;13(4):231-6.
Helicobacter pylori (Hp) infection influences cell metabolism and apoptosis in the epithelium and lymphocytes of gastric mucosa. It may cause difficulties in the elimination of bacteria and lead to chronic gastritis. THE AIM OF THE STUDY was to find if there is a relationship between periapoptotic markers such as Fas, FasL and Bcl-2 in gastric mucosa in children with chronic gastritis and with Hp infection.
Forty-nine children with chronic abdominal pain were included in the study. They, were divided into three groups: group I without Hp (22) group II with (27) Hp infection. Eleven children from the second group who had follow-up endoscopy after eradication therapy formed group III. Hp infection was confirmed by 4 different methods. The triple- drug treatment was applied. Tissue samples from the gastric mucosa were obtained, during upper gastrointestinal endoscopy, for microscopic evaluation (according to the Sydney classification) and immunohistochemistry. In the analysed groups the percentage of patients with periapoptotic markers (Fas, FasL, Bcl-2) was established. The Fas antigen was estimated by immunofluorescent and immunoenzymatic methods. The FasL I Bcl-2 receptors were evaluated by the immunoenzymatic method.
The expression of FasL and Bcl-2 receptors was found in all children without Hp infection. The expression of Fas antigen was less frequent in this group. The expression of Fas receptor was statistically significantly more frequent (p<0.05) in children with Hp infection. The expression of FasL and Bcl-2 in children with Hp infection was similar to group I (without Hp infection). In group of children after eradication treatment the expression of Fas and Bcl-2 (p<0.05) markers were significantly less frequent.
Helicobacter pylori activates apoptosis by two pathways. It appears that the Fas/FasL pathway is the main one. Only in the case of Fas receptor there is a link between its significantly more frequent expression with Hp infection and its reduction after eradication treatment.
幽门螺杆菌（Hp）感染会影响胃黏膜上皮细胞和淋巴细胞的细胞代谢及凋亡。它可能导致细菌清除困难并引发慢性胃炎。本研究的目的是探寻慢性胃炎伴Hp感染儿童胃黏膜中Fas、FasL和Bcl-2等凋亡相关标志物之间是否存在关联。
49名有慢性腹痛的儿童纳入本研究。他们被分为三组：第一组无Hp感染（22名），第二组有Hp感染（27名）。第二组中11名在根除治疗后接受随访内镜检查的儿童组成第三组。通过4种不同方法确诊Hp感染。采用三联药物治疗。在上消化道内镜检查期间获取胃黏膜组织样本，用于显微镜评估（根据悉尼分类法）和免疫组织化学检查。在分析的各组中确定具有凋亡相关标志物（Fas、FasL、Bcl-2）的患者百分比。通过免疫荧光和免疫酶法评估Fas抗原。通过免疫酶法评估FasL和Bcl-2受体。
在所有无Hp感染的儿童中均发现FasL和Bcl-2受体的表达。该组中Fas抗原的表达较少见。Fas受体的表达在Hp感染儿童中在统计学上显著更常见（p<0.05）。Hp感染儿童中FasL和Bcl-2的表达与第一组（无Hp感染）相似。在根除治疗后的儿童组中，Fas和Bcl-2（p<0.05）标志物的表达显著少见。
幽门螺杆菌通过两条途径激活凋亡。似乎Fas/FasL途径是主要途径。仅就Fas受体而言，其表达在Hp感染时显著更常见与根除治疗后降低之间存在关联。
