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Updated: Mar 13, 2026
Isolation and Profiling of MicroRNA-containing Exosomes from Human Bile
Published on: June 13, 2016
MicroRNA-155 in exosomes secreted from helicobacter pylori infection macrophages immunomodulates inflammatory
Jianjun Wang1, Zhiyong Deng1, Zeyou Wang2
1Department of Clinical Laboratory, Kunshan First People's Hospital, Affiliated to Jiangsu University Kunshan 215300, People's Republic of China.
Abstract:
Exosomes containing microRNA-155 act as molecule carriers during immune cell-cell communication and play an important role in the inflammatory response of H. pylori infection macrophages. Previous reports have found that miR-155 was over-expressed in H. pylori infection macrophages, but the significance of which is still unknown. In this study, we analyzed the impact of miR-155 loaded in exosomes derived from macrophages to the inflammatory response of H. pylori infection macrophages and possible mechanisms. We found that miR-155 promoted the expression of inflammatory cytokines including TNF-a, IL-6, IL-23, but also increased the expression of CD40, CD63, CD81, and MCH-I. Meanwhile, inflammatory signal pathways proteins, such as MyD88, NF-κB in H. pylori infection macrophages were down-regulated due to the over-expression of miR-155. Experiments in vitro or in vivo revealed that miR-155 promoted macrophages to inhibit or kill H. pylori by regulating the inflammatory response of cells to prevent the gastritis caused by H. pylori infection. These findings contribute to the understanding of miR-155 contained in exosomes in inflammatory responses of H. pylori infection macrophages.
Insights
MicroRNA-155 within exosomes influences macrophage inflammatory responses during Helicobacter pylori infection. This study reveals miR-155 promotes anti-H. pylori activity by modulating cellular inflammation.
Area of Science:
- Immunology
- Molecular Biology
- Microbiology
Background:
- Exosomes mediate intercellular communication, carrying microRNAs (miRNAs) like microRNA-155 (miR-155).
- miR-155 is over-expressed in macrophages during Helicobacter pylori infection, but its functional significance remains unclear.
- Understanding miR-155's role in H. pylori-induced inflammation is crucial for host defense.
Purpose of the Study:
- To investigate the impact of exosome-derived miR-155 on macrophage inflammatory responses to H. pylori.
- To elucidate the underlying mechanisms by which miR-155 affects H. pylori infection outcomes.
- To determine if miR-155 can modulate macrophage activity against H. pylori.
Main Methods:
- Analysis of exosome-derived miR-155 levels in H. pylori-infected macrophages.
- Assessment of inflammatory cytokine and cell marker expression (TNF-a, IL-6, IL-23, CD40, CD63, CD81, MCH-I).
- Evaluation of inflammatory signaling pathway proteins (MyD88, NF-κB) and in vitro/in vivo experiments to assess H. pylori inhibition/killing.
Main Results:
- Exosomal miR-155 promoted the expression of pro-inflammatory cytokines (TNF-a, IL-6, IL-23) and cell markers (CD40, CD63, CD81, MCH-I).
- Over-expression of miR-155 led to down-regulation of inflammatory signaling proteins MyD88 and NF-κB.
- miR-155 facilitated macrophage-mediated inhibition and killing of H. pylori, potentially preventing H. pylori-induced gastritis.
Conclusions:
- Exosomal miR-155 plays a significant role in regulating macrophage inflammatory responses during H. pylori infection.
- miR-155 enhances the host's ability to combat H. pylori infection by modulating inflammation.
- These findings offer insights into exosome-mediated communication in H. pylori pathogenesis and host defense.
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