EXPRESSION OF INTERLEUKIN-8 AND CD54 BY HUMAN GASTRIC EPITHELIUM AFTER HELICOBACTER-PYLORI INFECTION IN-VITRO
EXPRESSION OF INTERLEUKIN-8 AND CD54 BY HUMAN GASTRIC EPITHELIUM AFTER HELICOBACTER-PYLORI INFECTION IN-VITRO
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DOI：
10.1016/0016-5085(95)90009-8
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发表时间：
1995-01-01
期刊：
影响因子：
29.4
通讯作者：
ERNST, PB
中科院分区：
文献类型：
--
作者：
CROWE, SE;ALVAREZ, L;ERNST, PB
背景/目的：幽门螺杆菌与中性粒细胞浸润有关，尽管其募集机制仅部分明确。本研究的目的是确定人类胃上皮细胞系Kato III是否表达细胞因子和细胞间粘附分子1（ICAM-1），这可能有助于在感染H.幽门。方法：用H. pylori感染的证据，细胞因子的产生，和ICAM-1的表达进行了检查。结果如下：在感染H.幽门。感染的加藤III上清液激活中性粒细胞，表现为CD 11b/CD 18增加和L-选择素减少，可被抗白细胞介素8阻断。空肠弯曲菌脂多糖则能杀死H. pylori培养上清; pylori不增加白细胞介素8。白细胞介素2和6，干扰素α，β和γ，以及肿瘤坏死因子不产生休息或H。幽门刺激的Kato III细胞。除了产生白细胞介素8，加藤III组成型表达的表面ICAM-1，作为一种细胞间粘附分子的中性粒细胞。结论：我们的结果表明H.幽门螺杆菌刺激胃上皮以引发炎症和中性粒细胞募集和活化。
Background/Aims: Helicobacter pylori is associated with neutrophil infiltrates, although the mechanism of their recruitment is only partially defined. The aim of the study was to determine if Kato III, a human gastric epithelial cell line, expressed cytokines and the intercellular adhesion molecule 1 (ICAM-1), which could contribute to the initiation of inflammation during infection with H. pylori. Methods: Kato III cells were stimulated with H. pylori and were examined for evidence of infection, cytokine production, and the expression of ICAM-1. Results: The expression of interleukin 8 messenger RNA and immunoreactive protein by Kato III cells was significantly increased over constitutive levels within 3 hours of infection with H. pylori. Infected Kato III supernatants activated neutrophils as evidenced by increased CD11b/CD18 and decreased L-selectin that could be blocked by anti-interleukin 8. In contrast, Campylobacter jejuni, lipopolysaccharide, killed H. pylori, and supernatants from cultures of H. pylori did not increase interleukin 8. Interleukins 2 and 6; interferons alfa, beta, and gamma; and tumor necrosis factor were not produced by resting or H. pylori-stimulated Kato III cells. In addition to producing interleukin 8, Kato III constitutively expressed surface ICAM-1, which acts as an intercellular adhesion molecule for neutrophils. Conclusions: Our results indicate that H. pylori stimulates the gastric epithelium to initiate inflammation and neutrophil recruitment and activation.