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<p>Post-traumatic lymphedema is often managed as a mechanical drainage problem. We asked whether the chronic condition reflects a selectively sustained inflammatory–fibrotic state. Skin from patients with manifest post-traumatic lymphedema (<i>n</i> = 23, typically 1–2&#xa0;years post-injury) and controls (<i>n</i> = 10) underwent quantitative immunohistochemistry (% marker-positive cells per standardized dermal ROI) and Luminex multiplex profiling (technical duplicates; two-tailed statistics after Shapiro–Wilk). Lymphedema tissue showed depressed lymphatic endothelial signaling: lower LYVE-1 and podoplanin (each <i>q</i> &lt; 0.001) and reduced VEGFR-3 (<i>q</i> &lt; 0.001) versus controls; myeloperoxidase was also lower (<i>q</i> &lt; 0.05), while lipoxygenase was unchanged. Luminex revealed a selective pro-inflammatory core (IL-1β <i>q</i> &lt; 0.05, IL-6 <i>q</i> &lt; 0.01, TNF-α <i>q</i> &lt; 0.01), with no differences in IL-4, IL-10, IL-12p40, IL-13, IL-17A, or RANTES/CCL5. Chemotactic cues were increased (MCP-1 <i>q</i> &lt; 0.01, MIP-1α <i>q</i> &lt; 0.01), aligning with monocyte/macrophage recruitment. Fibrosis-linked growth factors were upregulated (TGF-β1/β2/β3 each <i>q</i> &lt; 0.01; PDGF-AA <i>q</i> &lt; 0.05), while PDGF-BB was unchanged. Together, histology and soluble profiling converge on three axes—innate inflammatory drive, myeloid chemotaxis, and fibrotic remodeling—co-existing with suppressed lymphangiogenic tone. In this cohort, integrated human tissue profiling supports the view that chronic post-traumatic lymphedema is a selectively sustained inflammatory–fibrotic state rather than a purely mechanical disorder, suggesting stage-adapted therapeutic avenues that are prospectively testable.</p>

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New therapeutic targets in treatment of post-traumatic lymphedema

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月3日

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  • Felix Reinkemeier,
  • Alexander Wolff,
  • Alexander Fiedler,
  • Christoph Wallner,
  • Marius Drysch,
  • Sonja Verena Schmidt,
  • Flemming Puscz,
  • Maria Füth,
  • Carsten Theiss,
  • Marcus Lehnhardt,
  • Björn Behr,
  • Johannes Maximilian Wagner

摘要

Post-traumatic lymphedema is often managed as a mechanical drainage problem. We asked whether the chronic condition reflects a selectively sustained inflammatory–fibrotic state. Skin from patients with manifest post-traumatic lymphedema (n = 23, typically 1–2 years post-injury) and controls (n = 10) underwent quantitative immunohistochemistry (% marker-positive cells per standardized dermal ROI) and Luminex multiplex profiling (technical duplicates; two-tailed statistics after Shapiro–Wilk). Lymphedema tissue showed depressed lymphatic endothelial signaling: lower LYVE-1 and podoplanin (each q < 0.001) and reduced VEGFR-3 (q < 0.001) versus controls; myeloperoxidase was also lower (q < 0.05), while lipoxygenase was unchanged. Luminex revealed a selective pro-inflammatory core (IL-1β q < 0.05, IL-6 q < 0.01, TNF-α q < 0.01), with no differences in IL-4, IL-10, IL-12p40, IL-13, IL-17A, or RANTES/CCL5. Chemotactic cues were increased (MCP-1 q < 0.01, MIP-1α q < 0.01), aligning with monocyte/macrophage recruitment. Fibrosis-linked growth factors were upregulated (TGF-β1/β2/β3 each q < 0.01; PDGF-AA q < 0.05), while PDGF-BB was unchanged. Together, histology and soluble profiling converge on three axes—innate inflammatory drive, myeloid chemotaxis, and fibrotic remodeling—co-existing with suppressed lymphangiogenic tone. In this cohort, integrated human tissue profiling supports the view that chronic post-traumatic lymphedema is a selectively sustained inflammatory–fibrotic state rather than a purely mechanical disorder, suggesting stage-adapted therapeutic avenues that are prospectively testable.