Immunotherapy · 2026
ELAVL1 increases macrophage M1 polarization via upregulating S100A8 to promote Crohn's disease progression.
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Jia Lin, Chen Yingtai, Lu Ying
Аннотация
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.
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.