What question did this study set out to answer?

To identify the priming mechanism that induces interleukin-1β transcription in macrophages during the development of atherosclerosis.

July 16, 2015ScienceOpen Access

Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis

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Authors

AWAnnika WarnatschKing's College London ΜΙΜαριάννα ΙωάννουThe Francis Crick Institute QWQian WangAnhui Provincial Center for Disease Control and Prevention

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Implication

Animal study reveals that cholesterol crystals trigger neutrophil extracellular traps to prime macrophage cytokine production in mice, indicating how sterile inflammation drives atherosclerosis.

Key Points

To identify the priming mechanism that induces interleukin-1β transcription in macrophages during the development of atherosclerosis.
Used a murine model of atherosclerosis to assess sterile inflammatory signaling pathways.
Investigated the interactions among cholesterol crystals, neutrophils, macrophages, and T helper 17 cells.
Cholesterol crystals acted as dual signals, functioning both as priming and danger triggers for interleukin-1β production.
Crystals stimulated neutrophils to generate neutrophil extracellular traps, which primed macrophages for cytokine secretion and activated T helper 17 cells to accelerate plaque immune recruitment.

Cite This Study

Warnatsch et al. (2015) studied this question.

synapsesocial.com/papers/69d7f2ce66a29169b4bed8ac https://doi.org/10.1126/science.aaa8064

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Implication

Animal study reveals that cholesterol crystals trigger neutrophil extracellular traps to prime macrophage cytokine production in mice, indicating how sterile inflammation drives atherosclerosis.

Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis

Discussion

Member takes

Implication

Key Points

Cite This Study

Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis

Discussion

Member takes

Implication

Key Points

Cite This Study

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