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<p>Many studies analyze tissue-resident or blood-borne leukocytes to monitor disease progression. We hypothesized that the microvasculature serves as a distinct site for immune cell activity. Here, we investigate microvascular leukocyte phenotypes before, during and after acute kidney injury (AKI) in mice, uncovering unique characteristics in the kidney, liver, and lung. Using single-cell sequencing, we identify several immune cells that were up to 100-fold expanded in the kidney vasculature, including macrophages, dendritic cells (DC), and B cells. Regeneration after AKI is characterized by sustained remodeling of the renal microvascular interface. Homeostatic microvascular C1q<sup>+</sup> macrophages withdraw from the vascular barrier which is subsequently repopulated by new subsets, including CD11c<sup>+</sup>F480<sup>+</sup> and CD11c<sup>+</sup>F480<sup>−</sup> cells. These newly arrived macrophages exhibit enhanced phagocytic activity toward circulating bacteria and secretion of tumor necrosis factor, pointing to maladaptive repair mechanisms after AKI. These data suggest organ- and disease-specific microvascular immune dynamics which are not detectable through conventional blood and tissue analysis.</p>

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Microvascular immunity is organ-specific and remodeled after kidney injury in mice

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月9日

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  • Rebecca Rixen,
  • Paula Schütz,
  • Carolin Walter,
  • Birte Hüchtmann,
  • Veerle Van Marck,
  • Barbara Heitplatz,
  • Julian Varghese,
  • Georg Varga,
  • Dirk Foell,
  • Thomas Pap,
  • Hermann Pavenstädt,
  • Konrad Buscher

摘要

Many studies analyze tissue-resident or blood-borne leukocytes to monitor disease progression. We hypothesized that the microvasculature serves as a distinct site for immune cell activity. Here, we investigate microvascular leukocyte phenotypes before, during and after acute kidney injury (AKI) in mice, uncovering unique characteristics in the kidney, liver, and lung. Using single-cell sequencing, we identify several immune cells that were up to 100-fold expanded in the kidney vasculature, including macrophages, dendritic cells (DC), and B cells. Regeneration after AKI is characterized by sustained remodeling of the renal microvascular interface. Homeostatic microvascular C1q+ macrophages withdraw from the vascular barrier which is subsequently repopulated by new subsets, including CD11c+F480+ and CD11c+F480− cells. These newly arrived macrophages exhibit enhanced phagocytic activity toward circulating bacteria and secretion of tumor necrosis factor, pointing to maladaptive repair mechanisms after AKI. These data suggest organ- and disease-specific microvascular immune dynamics which are not detectable through conventional blood and tissue analysis.