Noach L A, Bosma N B, Jansen J, Hoek F J, van Deventer S J, Tytgat G N
Dept. of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.
Scand J Gastroenterol. 1994 May;29(5):425-9. doi: 10.3109/00365529409096833.
We investigated whether tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and interleukin-8 (IL-8) are involved in the inflammatory reaction of Helicobacter pylori infection. In 23 patients with H. pylori infection and 16 patients with negative cultures for H. pylori and normal antral mucosa, the mucosal production of TNF-alpha, IL-1 beta, and IL-8 was measured in antral biopsy specimens after 23 h of in vitro culture. The levels of TNF-alpha and IL-1 beta appeared to be significantly higher in H. pylori-positive patients (p = 0.0002 for both TNF-alpha and IL-1 beta). IL-8 production was also higher in H. pylori-infected subjects, but this difference did not reach statistical significance (p = 0.057). No significant differences were found between the level of the cytokines in H. pylori-infected patients with or without duodenal ulcer disease. A strong correlation was found between the production of IL-1 beta and IL-8. The biologic effects of these cytokines may explain the conspicuous recruitment, influx, and activation of neutrophils in the gastric mucosa during H. pylori infection.
我们研究了肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-8（IL-8）是否参与幽门螺杆菌感染的炎症反应。在23例幽门螺杆菌感染患者和16例幽门螺杆菌培养阴性且胃窦黏膜正常的患者中，体外培养23小时后，测定胃窦活检标本中TNF-α、IL-1β和IL-8的黏膜产生量。幽门螺杆菌阳性患者的TNF-α和IL-1β水平似乎显著更高（TNF-α和IL-1β均为p = 0.0002）。幽门螺杆菌感染受试者的IL-8产生量也更高，但这种差异未达到统计学意义（p = 0.057）。在有或无十二指肠溃疡病的幽门螺杆菌感染患者中，细胞因子水平未发现显著差异。发现IL-1β和IL-8的产生之间存在强相关性。这些细胞因子的生物学效应可能解释了幽门螺杆菌感染期间胃黏膜中嗜中性粒细胞的明显募集、流入和激活。
