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<p>ME-2, a GXG’G’’M type polysaccharide with a high <i>O</i>-acetyl group content, was isolated and purified from <i>Auricularia auricula</i>-judae. However, the mechanism underlying its immunomodulatory activity has not been thoroughly investigated. This study demonstrates that ME-2 effectively reverses cyclophosphamide-induced immunosuppression in vivo by normalizing organ indices, increasing serum cytokine levels, and restoring the structure of the spleen tissue. In vitro, ME-2 binds to TLR4 on the surface of RAW264.7 cells. This binding triggered the activation of both the MAPK and NF-κB signaling pathways. Consequently, ME-2 treatment promoted the secretion of immune effector factors, enhanced endocytic activity, and induced a shift toward the M1 phenotype. Subsequently, the above mechanism was reversely validated through TLR4 knockdown and specific signaling pathway inhibitors. These results demonstrate that ME-2 exhibits a potent immune activation effect, laying a foundation for the development of ME-2-based immunomodulators. In addition, experimental results demonstrated that dME-2 with complete de-<i>O</i>-acetylation exhibits no binding affinity for TLR4 and fails to activate its downstream signaling pathways. These findings confirm that <i>O</i>-acetyl groups are indispensable for ME-2-mediated immune activation.</p> Graphical abstract <p></p>

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Acetyl group dictates macrophage immune activation by polysaccharide ME-2 via TLR4-NF-κB/MAPK pathways

  • 期刊论文

  • 发表日期：

    2026年7月20日

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  • Nan Wang,
  • Lan Zhou,
  • Si-Liang Jiang,
  • Wen-Fei Wang,
  • Hai-Xue Kuang,
  • Jun Liang,
  • Yong-Gang Xia

摘要

ME-2, a GXG’G’’M type polysaccharide with a high O-acetyl group content, was isolated and purified from Auricularia auricula-judae. However, the mechanism underlying its immunomodulatory activity has not been thoroughly investigated. This study demonstrates that ME-2 effectively reverses cyclophosphamide-induced immunosuppression in vivo by normalizing organ indices, increasing serum cytokine levels, and restoring the structure of the spleen tissue. In vitro, ME-2 binds to TLR4 on the surface of RAW264.7 cells. This binding triggered the activation of both the MAPK and NF-κB signaling pathways. Consequently, ME-2 treatment promoted the secretion of immune effector factors, enhanced endocytic activity, and induced a shift toward the M1 phenotype. Subsequently, the above mechanism was reversely validated through TLR4 knockdown and specific signaling pathway inhibitors. These results demonstrate that ME-2 exhibits a potent immune activation effect, laying a foundation for the development of ME-2-based immunomodulators. In addition, experimental results demonstrated that dME-2 with complete de-O-acetylation exhibits no binding affinity for TLR4 and fails to activate its downstream signaling pathways. These findings confirm that O-acetyl groups are indispensable for ME-2-mediated immune activation.

Graphical abstract