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Updated: May 5, 2026
Depletion and Reconstitution of Macrophages in Mice
Published on: August 1, 2012
ELAVL1 increases macrophage M1 polarization via upregulating S100A8 to promote Crohn's disease progression
Lin Jia1, Yingtai Chen2, Ying Lu3
1School of Basic Medicine, Jinzhou Medical University, Jinzhou, China.
Objective:
This study aims to investigate the impact and molecular mechanism of ELAVL1 in promoting macrophage M1 polarization in Crohn's disease (CD) by upregulating S100A8 expression.
Methods:
Peripheral blood mononuclear cells (PBMCs) from CD patients were collected to assess the expression of S100A8 and ELAVL1. The effect of ELAVL1/S100A8 on THP1 derived macrophage polarization and pro-inflammatory mediator secretion were evaluated via siRNA silencing and rescue experiments. RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays validated the interaction between ELAVL1 and S100A8.
Results:
Both S100A8 and ELAVL1 were significantly overexpressed in CD patients. Knockdown of S100A8 or ELAVL1 in M1-polarized macrophages marked reduced the expression of M1 biomarkers (CD80, CD86) and pro-inflammatory mediators. However, S100A8 overexpression reversed the inhibitory effects of ELAVL1 knockdown on M1 polarization, thereby promoting the M1 polarization and inflammatory response. RIP and RNA pull-down assays confirmed that ELAVL1 directly binds to S100A8 mRNA to regulate its expression.
Conclusion:
ELAVL1 promotes M1 polarization of macrophages to exacerbate intestinal inflammation in CD via up-regulating S100A8 expression. These findings highlight the ELAVL1/S100A8 axis as a potential therapeutic target or diagnostic biomarker for managing CD.
Insights
ELAVL1 promotes M1 macrophage polarization and intestinal inflammation in Crohn's disease (CD) by increasing S100A8. This ELAVL1/S100A8 pathway offers potential therapeutic targets for CD.
Area of Science:
- Immunology
- Gastroenterology
- Molecular Biology
Background:
- Crohn's disease (CD) is a chronic inflammatory bowel disease.
- Macrophage polarization, particularly M1 phenotype, contributes to intestinal inflammation in CD.
- The molecular mechanisms driving M1 polarization in CD remain incompletely understood.
Purpose of the Study:
- To investigate the role of ELAVL1 in macrophage M1 polarization in CD.
- To elucidate the molecular mechanism by which ELAVL1 influences S100A8 expression.
- To explore the therapeutic potential of targeting the ELAVL1/S100A8 axis in CD.
Main Methods:
- Collected peripheral blood mononuclear cells (PBMCs) from CD patients.
- Assessed S100A8 and ELAVL1 expression levels.
- Utilized siRNA silencing and rescue experiments to evaluate ELAVL1/S100A8 effects on macrophage polarization and cytokine secretion.
- Performed RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays to confirm direct interaction.
Main Results:
- ELAVL1 and S100A8 were significantly overexpressed in CD patients.
- Knockdown of ELAVL1 or S100A8 reduced M1 biomarkers (CD80, CD86) and pro-inflammatory mediators.
- S100A8 overexpression rescued the inhibitory effects of ELAVL1 knockdown on M1 polarization.
- ELAVL1 directly binds to S100A8 mRNA, regulating its expression.
Conclusions:
- ELAVL1 promotes M1 macrophage polarization and exacerbates intestinal inflammation in CD by upregulating S100A8.
- The ELAVL1/S100A8 axis is a potential therapeutic target and diagnostic biomarker for CD management.
