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CpG-ODN enhances ingestion of apoptotic neutrophils by macrophages

Jiong Wang1, Wei-Lin Huang, Rong-Yu Liu

  • 1Department of Pulmonary, Anhui Geriatrics Institute, The First Affiliated Hospital of Anhui Medical University, Jixi Road 218, 230022, Hefei, People's Republic of China.

Clinical and Experimental Medicine
|October 28, 2008
PubMed

Insights

Synthetic oligodeoxynucleotides containing CpG motifs (CpG-ODN) enhance macrophage ingestion of apoptotic neutrophils via Toll-like receptor 9 (TLR9). This process involves increased TNF-alpha, which is subsequently down-regulated after phagocytosis.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Macrophage phagocytosis of apoptotic neutrophils is crucial for resolving inflammation.
  • Toll-like receptor 9 (TLR9) recognizes CpG motifs in microbial DNA and plays a role in immune responses.

Purpose of the Study:

  • To investigate the effect of CpG-oligodeoxynucleotides (CpG-ODN) on macrophage phagocytosis of apoptotic neutrophils in vitro.
  • To elucidate the role of Toll-like receptor 9 (TLR9) in this process and its impact on cytokine production.

Main Methods:

  • Macrophages were stimulated with CpG-ODN, and their ability to ingest apoptotic neutrophils was assessed.
  • TLR9 expression levels were analyzed.
  • The effect of chloroquine (CHQ), an inhibitor of endosomal acidification, on phagocytosis and cytokine production was evaluated.

Main Results:

  • CpG-ODN stimulation significantly increased the percentage of macrophages ingesting apoptotic neutrophils.
  • This effect was dependent on CpG motifs and mediated through TLR9.
  • CpG-ODN upregulated TLR9 expression and induced TNF-alpha production, which was inhibited by CHQ and down-regulated after phagocytosis.

Conclusions:

  • CpG-ODN enhances macrophage phagocytosis of apoptotic neutrophils via TLR9.
  • The process involves TLR9-mediated TNF-alpha production, which is downregulated upon phagocytosis of apoptotic neutrophils.
  • Further studies are needed to understand the implications for immune response regulation.

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