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Updated: Jun 29, 2025

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Differential cytokine expression in gastric tissues highlights helicobacter pylori's role in gastritis
Xing-Tang Yang1,2, Pei-Qin Niu3, Xiao-Feng Li4
1Department of Gastroenterology, Chongming Branch, Shanghai Tenth People's Hospital, Tongji University School of Medicine, No. 66 Xiangyangdong Road, Bao Town, Chongming District, Shanghai, 202157, People's Republic of China. yxtmg210@163.com.
Abstract:
Helicobacter pylori (H. pylori), known for causing gastric inflammation, gastritis and gastric cancer, prompted our study to investigate the differential expression of cytokines in gastric tissues, which is crucial for understanding H. pylori infection and its potential progression to gastric cancer. Focusing on Il-1β, IL-6, IL-8, IL-12, IL-18, and TNF-α, we analysed gene and protein levels to differentiate between H. pylori-infected and non-infected gastritis. We utilised real-time quantitative polymerase chain reaction (RT-qPCR) for gene quantification, immunohistochemical staining, and ELISA for protein measurement. Gastric samples from patients with gastritis were divided into three groups: (1) non-gastritis (N-group) group, (2) gastritis without H. pylori infection (G-group), and (3) gastritis with H. pylori infection (GH-group), each consisting of 8 samples. Our findings revealed a statistically significant variation in cytokine expression. Generally, cytokine levels were higher in gastritis, but in H. pylori-infected gastritis, IL-1β, IL-6, and IL-8 levels were lower compared to H. pylori-independent gastritis, while IL-12, IL-18, and TNF-α levels were higher. This distinct cytokine expression pattern in H. pylori-infected gastritis underscores a unique inflammatory response, providing deeper insights into its pathogenesis.
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