<i>Chlorella pyrenoidosa</i> Polysaccharide CPP-3a Promotes M1 Polarization of Macrophages via TLR4/2-MyD88-NF-κB/p38 MAPK Signaling Pathways

The immunomodulatory polysaccharide CPP-3a, purified from <i>Chlorella pyrenoidosa</i>, was investigated for its effects on RAW264.7 macrophages and underlying mechanisms, revealing that CPP-3a significantly enhanced phagocytic capacity and nitric oxide production while upregulating pro-...

Full description

Saved in:
Bibliographic Details
Main Authors: Yihua Pi, Qingxia Yuan, Shaoting Qin, Chundie Lan, Qingdong Nong, Chenxia Yun, Haibo Tang, Jing Leng, Jian Xiao, Longyan Zhao, Lifeng Zhang
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Marine Drugs
Subjects:
Online Access:https://www.mdpi.com/1660-3397/23/7/290
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The immunomodulatory polysaccharide CPP-3a, purified from <i>Chlorella pyrenoidosa</i>, was investigated for its effects on RAW264.7 macrophages and underlying mechanisms, revealing that CPP-3a significantly enhanced phagocytic capacity and nitric oxide production while upregulating pro-inflammatory cytokines TNF-α and IL-6 and elevating the co-stimulatory molecule CD86, collectively driving robust M1 polarization. Mechanistically, TLR4-, TLR2-specific inhibitors, and TLR4-knockout cells confirmed TLR4 as the primary receptor for CPP-3a, with TLR2 playing a secondary role in cytokine modulation. CPP-3a activated NF-κB and p38 MAPK signaling pathways via the MyD88-dependent pathway, evidenced by phosphorylation of NF-κB/p65 with its nuclear translocation and increased phosphorylation of p38 MAPK, with these signaling activations further validated by specific pathway inhibitors that abolished M1 polarization phenotypes. Collectively, CPP-3a emerges as a potent TLR4-targeted immunomodulator with adjuvant potential for inflammatory and infectious diseases.
ISSN:1660-3397