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Vikram Sabapathy1, Gabrielle Costlow1,2, Saanvi Acharya1,3

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The interleukin-33 (IL-33) and ST2 pathway regulates macrophage function in kidney injury. Loss of ST2 impairs macrophage metabolism and efferocytosis, impacting tissue repair and homeostasis.

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Area of Science:

  • Immunology
  • Renal Physiology
  • Cell Biology

Background:

  • Innate immune cells, particularly macrophages, are crucial in kidney injury responses.
  • The IL-33/ST2 signaling pathway is implicated in inflammation and tissue repair.
  • The precise role of ST2 in macrophage function during kidney injury remains unclear.

Purpose of the Study:

  • To investigate the role of ST2 in myeloid cells during acute and chronic kidney ischemia-reperfusion injury (IRI).
  • To elucidate the mechanisms by which ST2 influences macrophage function, metabolism, and efferocytosis.

Main Methods:

  • Utilized myeloid cell-specific ST2 knockout mice (ST2 fl/fl .LysM Cre) in acute and chronic IRI models.
  • Assessed kidney structure and function via histology, flow cytometry, and gene expression analysis.
  • Investigated macrophage function in vitro using efferocytosis assays, RNA sequencing, and Seahorse metabolic analysis.

Main Results:

  • ST2 deletion attenuated acute IRI but exacerbated chronic IRI, indicating a dual role in injury resolution.
  • RNA sequencing revealed downregulated genes related to oxidative phosphorylation and efferocytosis in ST2-deficient macrophages.
  • ST2-deficient macrophages exhibited reduced phagocytic activity and compromised mitochondrial metabolism.

Conclusions:

  • The IL-33/ST2 axis is critical for regulating macrophage function and metabolic activity.
  • ST2 signaling is essential for effective efferocytosis and tissue homeostasis following renal injury.
  • Targeting the IL-33/ST2 pathway may offer therapeutic potential for kidney injury management.