Related Experiment Video
Updated: Sep 22, 2025

Injections of Lipopolysaccharide into Mice to Mimic Entrance of Microbial-derived Products After Intestinal Barrier Breach
Published on: May 2, 2018
Methyltransferase like 7B is upregulated in sepsis and modulates lipopolysaccharide-induced inflammatory response and
Abstract:
Macrophages play a critical role in the regulation of the inflammatory responses in sepsis. Methyltransferase like 7B (METTL7B) has been implicated in several pathophysiological conditions. Nevertheless, the potential engagement of METTL7B in sepsis remains to be elucidated. In this study, we retrieved transcriptomic profile data of septic patients and healthy donors and compared the expression level of METTL7B between septic patients and healthy controls. We also collected septic patient samples to analyze METTL7B expression via RT-qPCR. Murine bone marrow-derived macrophages (BMDMs) were isolated and treated with incremental doses of LPS as an in vitro cell model. METTL7B was overexpressed or knocked down in BMDMs, and lipopolysaccharide (LPS)-mediated inflammatory cytokines production and macrophage polarization were evaluated. We found that METTL7B was upregulated in the blood and peripheral blood mononuclear cells (PBMC) of septic patients, which also showed a significant diagnostic potential for sepsis. In BMDMs, METTL7B was induced in a time and dose-dependent manner by LPS. Modulating the expression level of METTL7B could regulate LPS-mediated inflammatory cytokines production and macrophage polarization. The functional role of METTL7B was also validated in a septic mouse model. Our findings indicate that METTL7B is implicated in the immunopathogenesis of sepsis through modulating macrophage-mediated inflammatory responses. METTL7B may serve as a potential diagnostic and therapeutic target for sepsis.
Insights
Methyltransferase like 7B (METTL7B) is upregulated in sepsis patients and regulates inflammatory responses in macrophages. METTL7B shows diagnostic potential and may be a therapeutic target for sepsis.
Area of Science:
- Immunology
- Molecular Biology
- Pathophysiology
Background:
- Macrophages are key regulators of inflammatory responses in sepsis.
- Methyltransferase like 7B (METTL7B) is involved in various pathophysiological conditions.
- The role of METTL7B in sepsis pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the expression and function of METTL7B in sepsis.
- To determine if METTL7B plays a role in macrophage-mediated inflammatory responses during sepsis.
- To explore METTL7B as a potential diagnostic and therapeutic target for sepsis.
Main Methods:
- Analysis of transcriptomic data from septic patients and healthy donors.
- Quantitative reverse transcription PCR (RT-qPCR) on patient samples.
- In vitro studies using murine bone marrow-derived macrophages (BMDMs) stimulated with lipopolysaccharide (LPS).
- Overexpression and knockdown of METTL7B in BMDMs.
- Evaluation of inflammatory cytokines and macrophage polarization.
- Validation in a septic mouse model.
Main Results:
- METTL7B expression was significantly upregulated in septic patients' blood and PBMCs, indicating diagnostic potential.
- LPS treatment induced METTL7B expression in BMDMs in a time- and dose-dependent manner.
- Modulating METTL7B levels affected LPS-induced inflammatory cytokine production and macrophage polarization.
- METTL7B's role was confirmed in a septic mouse model.
Conclusions:
- METTL7B is upregulated in sepsis and contributes to the immunopathogenesis by modulating macrophage-mediated inflammatory responses.
- METTL7B may serve as a valuable diagnostic biomarker for sepsis.
- METTL7B represents a potential therapeutic target for managing sepsis.
More Related Videos
07:45Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
Published on: November 28, 2015
11:48Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018