{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:59:13Z","timestamp":1787018353444,"version":"build-2736575974"},"reference-count":83,"publisher":"American Society for Clinical Investigation","issue":"7","license":[{"start":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T00:00:00Z","timestamp":1775606400000},"content-version":"vor","delay-in-days":34,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["PO1-HL151327,PO1-HL160469,RO1-HL137169,RO1-155941,RO1-HL084153,RO1-HL165263"],"award-info":[{"award-number":["PO1-HL151327,PO1-HL160469,RO1-HL137169,RO1-155941,RO1-HL084153,RO1-HL165263"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,4,8]]},"abstract":"<jats:p>\n                    Aberrant polymorphonuclear neutrophil (PMN) accumulation in tissues induces chronic vascular diseases. Endothelial cells (ECs) regulate the access of PMNs into the tissue from the blood. However, the mechanisms that prevent PMNs from being activated and accumulating in the tissue, a hallmark of acute lung injury (ALI), remain elusive. We demonstrate that conditional deletion of\n                    <jats:italic>Erg<\/jats:italic>\n                    in ECs spontaneously alters the PMN transcriptome, which is enriched with genes that induce PMN recruitment, adhesion, activation, and \u201cdo not eat me\u201d signals due to impaired synthesis of the deubiquitinase A20. Decreased A20 levels, in turn, activated the transcription factor NF-\u03baB and the secretion of MIP2\u03b1 (human homolog of IL-8) in ECs. EC-secreted MIP2\u03b1\/IL-8 engaged the CXCR2 cascade on PMNs, leading to their activation and inflammatory injury. These findings were recapitulated in the lungs and blood of PMNs from patients dying of ALI. Overexpression of the\n                    <jats:italic>A20<\/jats:italic>\n                    gene in ECs or pharmacological inhibition of CXCR2 on PMNs in\n                    <jats:italic>\n                      iEC-Erg\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice rescued EC control of PMNs and tissue homeostasis, and enhanced mouse survival after pneumonia. Thus, the EC\/Erg\/A20 axis regulates PMN accumulation and hyperactivation in the lungs by inhibiting EC-mediated IL-8 activation of PMN CXCR2, thereby providing a potential target for neutrophilic inflammatory vascular diseases.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.195989","type":"journal-article","created":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T17:00:26Z","timestamp":1772730026000},"source":"Crossref","is-referenced-by-count":1,"title":["ERG-deficient endothelium identifies IL-8\/CXCR2 axis as a therapeutic target for resolving neutrophilic lung vascular injury"],"prefix":"10.1172","volume":"11","author":[{"given":"Vigneshwaran","family":"Vellingiri","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Regenerative Medicine, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vijay Avin Balaji","family":"Ragunathrao","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Regenerative 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