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Nuclear HMGB1 promotes the phagocytic ability of macrophages

Jifei Miao1, Sen Ye1, Jiao Lan2

  • 1Research Center of Integrative Medicine, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, PR China.

Experimental Cell Research
|May 4, 2020
PubMed

Insights

Nuclear High Mobility Group Protein B1 (HMGB1) enhances macrophage phagocytosis by interacting with P53 and promoting focal adhesion kinase (FAK) phosphorylation, boosting immune response to pathogens.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Phagocytosis is a critical immune mechanism against pathogens.
  • High Mobility Group Protein B1 (HMGB1), a DNA chaperone, is linked to phagocytosis, but its role is debated.
  • Understanding HMGB1's function in phagocytosis is crucial for immune response research.

Purpose of the Study:

  • To investigate the influence of High Mobility Group Protein B1 (HMGB1) on macrophage phagocytic function.
  • To elucidate the molecular mechanisms by which HMGB1 affects phagocytosis.
  • To determine the role of nuclear HMGB1 in modulating immune responses.

Main Methods:

  • Construction of HMGB1-mutant, -overexpressing, and -silenced RAW264.7 cell lines.
  • Generation of HMGB1 conditional knockout mice for in vivo studies.
  • Stimulation with lipopolysaccharide (LPS) to induce HMGB1 translocation and zymosan particles to assess phagocytosis.

Main Results:

  • Nuclear accumulation of HMGB1 significantly enhances macrophage phagocytic activity.
  • HMGB1 interacts with P53, potentially reducing P53's inhibitory effect on focal adhesion kinase (FAK) phosphorylation.
  • Increased phosphorylated FAK promotes pseudopod formation, thereby enhancing phagocytosis.

Conclusions:

  • Nuclear HMGB1 plays a key role in enhancing macrophage phagocytosis.
  • The interaction between HMGB1 and P53 is a critical factor in regulating FAK phosphorylation and phagocytic capacity.
  • Targeting nuclear HMGB1 could be a strategy to augment immune responses against pathogens.
Keywords:
FAKHMGB1MacrophageP53Phagocytosis

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