PBMC-derived FGF, PDGF, VEGF and GM-CSF secretion in endometriosis: a case–control in vitro study

Marcin Sadłocha, Aleksandra Krzywon, Jakub Marcin Staniczek, Jakub Toczek, Zenon Czuba, Rafal Stojko
In: Frontiers in Medicine · 2026 · vol. 13 · doi:10.3389/fmed.2026.1821695 · W7163590750
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Peripheral blood mononuclear cells from women with endometriosis do not show increased in vitro secretion of FGF, PDGF, VEGF, and GM-CSF compared to controls.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This case–control study compared in vitro secretion of fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), and granulocyte–macrophage colony-stimulating factor (GM-CSF) by peripheral blood mononuclear cells (PBMCs) from 36 women with laparoscopically and histopathologically confirmed endometriosis versus 44 laparoscopic controls without visible endometriosis, under basal conditions and after nonspecific mitogenic stimulation with phytohemagglutinin (PHA). Baseline PBMC secretion of all four mediators did not significantly differ between groups after correction for multiple comparisons, and PHA-induced changes in secretion profiles were similar between groups after false discovery rate adjustment. Logistic regression using baseline growth-factor measures also found no significant predictors of endometriosis status. The study’s limitations include its reliance on unfractionated PBMCs, a single 24-hour culture timepoint, and the exploratory nature of mechanistic inference. This paper is centrally about endometriosis — it directly tests whether PBMCs from women with endometriosis have an intrinsically increased ex vivo secretory capacity for key pro-angiogenic and hematopoietic growth factors.

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Abstract

Background Endometriosis is a chronic inflammatory disease with immune dysregulation in which angiogenic, and hematopoietic mediators are thought to contribute to ectopic lesion establishment and persistence. Whether circulating immune cells are intrinsically primed to secrete higher levels of pro-angiogenic growth factors remains unclear. This study evaluated in vitro secretion of fibroblast growth factor (FGF), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF) and granulocyte–macrophage colony-stimulating factor (GM-CSF) by peripheral blood mononuclear cells (PBMCs) from women with and without endometriosis. Methods In a case–control design, women with laparoscopically and histopathologically confirmed endometriosis ( n = 36) and laparoscopically confirmed controls without endometriosis ( n = 44) were enrolled. PBMCs were isolated from peripheral blood and cultured for 24 h under basal conditions or after non-specific mitogenic activation with phytohemagglutinin (PHA, 5 μg/mL). Supernatant concentrations of FGF, PDGF, VEGF and GM-CSF were quantified using a multiplex bead-based immunoassay (Bio-Plex/Luminex). Between-group comparisons used nonparametric tests; univariate logistic regression explored associations with endometriosis status; and false discovery rate (Benjamini–Hochberg) adjustment was applied for multiple testing. Results Baseline secretion of FGF, PDGF, VEGF and GM-CSF by PBMCs did not differ significantly between women with endometriosis and controls after correction for multiple comparisons. PHA stimulation induced marked shifts in secretion profiles across participants— characterized by increases in FGF, PDGF and VEGF and a decrease in GM-CSF—but neither stimulated concentrations nor percent changes differed significantly between groups following false discovery rate adjustment. In univariate logistic regression analyses, none of the baseline growth-factor measures significantly predicted the presence of endometriosis. Conclusion Under standardized in vitro culture conditions, PBMCs from women with endometriosis do not show a generalized increase in secretory capacity for the evaluated pro-angiogenic/hematopoietic growth factors compared with PBMCs from controls without endometriosis. These data do not support systemic PBMC hypersecretion of FGF, PDGF, VEGF and GM-CSF in endometriosis and are consistent with a compartmentalized model in which disease-relevant pro-angiogenic signaling is predominantly shaped within local peritoneal and lesion microenvironments.

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endometriosis

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