{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T04:16:37Z","timestamp":1787026597127,"version":"build-2736575974"},"reference-count":75,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T00:00:00Z","timestamp":1783641600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Monocyte\u2013endothelial interactions drive both acute inflammation and chronic vascular disease in type 2 diabetes mellitus (T2DM), yet whether TNF-\u03b1\u2013induced and diabetes-associated monocyte trafficking engage similar or distinct molecular programs remains unclear. Using a physiological flow-based imaging system, we quantified CD14\n                    <jats:sup>+<\/jats:sup>\n                    monocyte adhesion, transendothelial migration (TEM), and abluminal residence on HUVEC monolayers activated with TNF-\u03b1 or T2DM serum under controlled shear stress. Both stimuli induced comparable monocyte adhesion (~40 cells by 3\u00a0min), but TEM efficiency diverged markedly: TNF-\u03b1 promoted robust TEM (~18% by 5\u00a0min) whereas T2DM conditions showed severely impaired TEM (~5%). Under T2DM conditions, monocytes exhibited prolonged abluminal retention (median 85\u00a0min vs. 25\u00a0min; p&amp;lt;0.0001), a phenotype recapitulated by endothelial hyperglycemic exposure alone. Comparative RNA-seq analysis of T2DM (GSE92724) and TNF-\u03b1\u2013stimulated (GSE134489) endothelial cells revealed near-zero transcriptional correlation (r = 0.018) between conditions. TNF-\u03b1 drove coordinate NF-\u03baB\u2013dependent upregulation of VCAM1, ICAM1, E-selectin, and junctional molecules with organized junctional remodeling, whereas T2DM produced VCAM1-biased adhesion with ICAM1 downregulation (0.61-fold), claudin suppression, and junctional disorganization. KEGG pathway mapping confirmed organized endothelial\u2013leukocyte integrin co-activation under TNF-\u03b1 versus discoordination junctional loss under T2DM. qPCR validation identified selective RAGE and JAM3 upregulation under T2DM\u2014consistent with AGE-RAGE signaling and JAM-3\u2013MAC-1 monocyte trapping\u2014without classical NF-\u03baB activation. These findings define two fundamentally distinct paradigms: a TNF-\u03b1 \u201crecruitment model\u201d enabling efficient trafficking and resolution, versus a T2DM \u201cretention model\u201d characterized by VCAM1-biased adhesion, junctional disorganization, and impaired reverse transmigration driving chronic monocyte accumulation, identifying AGE-RAGE signaling and JAM-3\u2013MAC-1 interactions as potential therapeutic targets for diabetic vascular inflammation.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1827607","type":"journal-article","created":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T04:25:23Z","timestamp":1783657523000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Flow-based imaging reveals dissociated monocyte adhesion and transmigration patterns between TNF-\u03b1 and diabetes-induced vascular inflammation"],"prefix":"10.3389","volume":"17","author":[{"given":"Dilvin","family":"Semo","sequence":"first","affiliation":[{"name":"Vascular Signaling, Molecular Cardiology, Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]},{"name":"Department of Cardiology I- Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohe","family":"Liang","sequence":"additional","affiliation":[{"name":"Vascular Signaling, Molecular Cardiology, Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariel","family":"Schwietzer","sequence":"additional","affiliation":[{"name":"Vascular Signaling, Molecular Cardiology, Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]},{"name":"Department of Cardiology I- Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weiqi","family":"Wang","sequence":"additional","affiliation":[{"name":"Vascular Signaling, Molecular Cardiology, Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaokang","family":"Hu","sequence":"additional","affiliation":[{"name":"Vascular Signaling, Molecular Cardiology, Department of Cardiology I - Coronary and Peripheral Vascular Disease, Heart Failure, University Hospital M\u00fcnster","place":["M\u00fcnster, 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