Inflammatory response of macrophages cultured with Helicobacter pylori strains was regulated by miR-155
Yongliang Yao1, Guangxin Li2, Jianhong Wu1
1Department of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University Kunshan 215300, People's Republic of China.
Abstract:
MicroRNA-155 plays an important role in the inflammatory response macrophages, while present studies identified that miR-155 was up-expressed in gastritis induced by Helicobacter pylori. We found that miR-155 was over expressed in macrophages infected with H. pylori in vivo or in vitro. Subsequently, inflammatory cytokines IL-23, IL-10, TNF-α and IL-8 were increased significantly, and the expression of CD80, CD86 or COX2, NOS2. Were enhanced in H. pylori infection macrophages by regulated with miR-155mimics. Furthermore, the apoptosis of macrophages induced by H. pylori was increased obviously due to the over-expression of miR-155. Therefore, these observations indicated that miR-155 may act as a inflammatory promoter in H. pylori infected macrophages. These findings contribute us to understand the functions of miR-155 in gastritis induced by H. pylori furtherly.
Insights
MicroRNA-155 (miR-155) promotes inflammation in macrophages during Helicobacter pylori infection. Overexpression of miR-155 increases inflammatory cytokines and macrophage apoptosis, suggesting its role in H. pylori-induced gastritis.
Area of Science:
- Immunology
- Molecular Biology
- Microbiology
Background:
- MicroRNA-155 (miR-155) is implicated in inflammatory responses.
- Previous studies suggest miR-155 is upregulated in Helicobacter pylori-induced gastritis.
- H. pylori infection is a major cause of gastritis and peptic ulcers.
Purpose of the Study:
- To investigate the role of miR-155 in macrophages during H. pylori infection.
- To determine the effect of miR-155 on inflammatory responses and apoptosis in H. pylori-infected macrophages.
Main Methods:
- Assessing miR-155 expression in H. pylori-infected macrophages in vitro and in vivo.
- Using miR-155 mimics to evaluate the impact on inflammatory cytokine and marker expression.
- Analyzing macrophage apoptosis following H. pylori infection and miR-155 manipulation.
Main Results:
- miR-155 was significantly overexpressed in macrophages infected with H. pylori.
- Upregulation of miR-155 led to increased levels of inflammatory cytokines (IL-23, IL-10, TNF-α, IL-8).
- miR-155 overexpression enhanced the expression of CD80, CD86, COX2, and NOS2, and promoted macrophage apoptosis.
Conclusions:
- miR-155 acts as a pro-inflammatory factor in macrophages during H. pylori infection.
- miR-155 contributes to the pathogenesis of H. pylori-induced gastritis.
- Targeting miR-155 may offer a therapeutic strategy for H. pylori-related gastric diseases.
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