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Exosomal secreted SCIMP regulates communication between macrophages and neutrophils in pneumonia

Xiaolei Pei1,2, Li Liu3,4, Jieru Wang3,4

  • 1State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Haihe Laboratory of Cell Ecosystem, Hematopoietic Stem Cell Transplantation Center, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, 300020, P. R. China. peixiaolei@ihcams.ac.cn.

Nature Communications
|January 23, 2024
PubMed

Insights

Macrophages secrete SCIMP exosomes that enhance neutrophil recruitment, improving survival in acute lung injury (ALI). This macrophage-SCIMP-formyl peptide receptor (FPR)-neutrophil axis is crucial for innate immunity in ALI.

Area of Science:

  • Immunology
  • Cell Biology
  • Pulmonology

Background:

  • Deficient pathogen clearance in pneumonia can cause acute lung injury (ALI) due to overactive immune responses.
  • SLP adaptor and CSK interacting membrane protein (SCIMP) exhibits neutrophil chemotactic activity during ALI, but its role is unclear.

Purpose of the Study:

  • To investigate the role of SCIMP secreted in exosomes (SCIMPexo) by macrophages in the pathogenesis of ALI.
  • To elucidate the mechanism by which SCIMP influences neutrophil activity and survival in ALI.

Main Methods:

  • Assessed SCIMPexo levels in bronchoalveolar lavage fluid and serum from pneumonia patients.
  • Investigated the effect of SCIMPexo and SCIMP N-terminal peptides on ALI survival in mouse models.
  • Utilized exosome suppressors and formyl peptide receptor 1/2 (FPR1/2) antagonists to evaluate the SCIMP-FPR pathway.
  • Compared survival rates of Scimp-deficient and Fpr1/2-deficient mice with wild-type controls.

Main Results:

  • SCIMPexo levels were significantly elevated in pneumonia patients.
  • Bronchial perfusion with SCIMPexo or peptides increased ALI model survival by attracting and activating neutrophils via FPR1/2.
  • Exosome suppressors and FPR1/2 antagonists reduced survival in a lethal ALI model.
  • Scimp-deficient and Fpr1/2-deficient mice exhibited lower survival rates.

Conclusions:

  • The macrophage-SCIMP-FPRs-neutrophil axis is a critical component of the innate immune response in ALI.
  • SCIMPexo plays a protective role in ALI by mediating neutrophil recruitment and activation.
  • Targeting the SCIMP-FPR pathway may offer therapeutic potential for treating ALI.

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