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Bidirectional regulation of neutrophil migration by mitogen-activated protein kinases

Xiaowen Liu1, Bo Ma, Asrar B Malik

  • 1Department of Dermatology, University of Illinois College of Medicine, Chicago, Illinois, USA.

Nature Immunology
|March 27, 2012
PubMed

Insights

Neutrophil migration is controlled by two opposing mitogen-activated protein kinases (MAPKs). Erk inhibits movement, while p38 promotes it, balancing neutrophil stop-and-go activity for effective host defense.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Neutrophils are crucial for host defense against bacterial invasion.
  • Neutrophil migration involves sensing spatial cues and reaching target sites.
  • While migration initiation is well-studied, the mechanisms terminating neutrophil movement are less understood.

Purpose of the Study:

  • To investigate the roles of mitogen-activated protein kinases (MAPKs) in regulating neutrophil trafficking.
  • To elucidate the molecular mechanisms controlling the termination of neutrophil chemotactic migration.

Main Methods:

  • Investigated the roles of extracellular signal-regulated kinase (Erk) and p38 MAPKs in neutrophil migration.
  • Examined the interaction between MAPKs and G protein-coupled receptor kinase 2 (GRK2).
  • Analyzed the phosphorylation of the formyl peptide receptor (FPR1) by p38.

Main Results:

  • Erk potentiated GRK2 activity, thereby inhibiting neutrophil migration.
  • p38 MAPK acted as a noncanonical GRK, phosphorylating FPR1 and blocking GRK2.
  • This phosphorylation facilitated neutrophil migration.
  • The balance between Erk and p38 activity regulated neutrophil 'stop' and 'go' dynamics.

Conclusions:

  • Dynamic interplay between Erk and p38 MAPKs governs neutrophil migration termination.
  • This balance ensures neutrophils effectively reach sites of infection as the first line of defense.
  • Understanding these pathways offers insights into immune cell trafficking and host defense mechanisms.

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