{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T05:00:16Z","timestamp":1785214816723,"version":"3.55.0"},"reference-count":65,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T00:00:00Z","timestamp":1781568000000},"content-version":"vor","delay-in-days":15,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T00:00:00Z","timestamp":1780272000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Physiological Reports"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Platelets are responsible for maintaining vascular integrity through the process of hemostasis with glycoprotein VI (GPVI) acting as a major receptor for platelet activation. Interestingly, platelet participation in inflammation is an evolving concept with few studies exploring GPVI in the framework of inflammation and even less in the context of the most severe inflammatory condition: sepsis. Here we utilized a GPVI deficient mouse model (GPVI\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) to elucidate the role of GPVI in the formation of circulating platelet\u2010leukocyte aggregates (PLAs) and how GPVI driven modifications impact leukocyte phenotype and function under septic systemic inflammatory conditions. Using the cecal ligation and puncture (CLP) technique to model sepsis in male mice, we report GPVI\u2010mediated modification of several inflammatory characteristics. GPVI deficiency reduced platelet adhesion to neutrophils and monocytes during sepsis, resulting in reduced neutrophil and increased monocyte activation. Furthermore, monocytes exhibited altered polarization with GPVI deletion, raising the levels of circulating non\u2010classical monocytes. The loss of GPVI also elicited a significant reduction in the levels of circulating TNF\u03b1. Finally, sepsis\u2010induced mortality was significantly exacerbated as survival was dramatically reduced in GPVI\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice over a five\u2010day period. These findings suggest that platelet GPVI impacts the inflammatory response during sepsis in a previously undocumented manner.\n                  <\/jats:p>","DOI":"10.14814\/phy2.70971","type":"journal-article","created":{"date-parts":[[2026,6,17]],"date-time":"2026-06-17T06:32:55Z","timestamp":1781677975000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Platelet glycoprotein\n                    <scp>VI<\/scp>\n                    modulates leukocyte characteristics in sepsis\u2010induced systemic inflammatory response in male mice"],"prefix":"10.14814","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4700-9091","authenticated-orcid":false,"given":"Adam","family":"Corken","sequence":"first","affiliation":[{"name":"Department of Pediatrics University of Arkansas for Medical Sciences  Little Rock Arkansas USA"},{"name":"Arkansas Children's Research Institute  Little Rock Arkansas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerry","family":"Ware","sequence":"additional","affiliation":[{"name":"Department of Physiology and Cell Biology University of Arkansas for Medical Sciences  Little Rock Arkansas USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6799-1203","authenticated-orcid":false,"given":"Keshari M.","family":"Thakali","sequence":"additional","affiliation":[{"name":"Department of Pediatrics University of Arkansas for Medical Sciences  Little Rock Arkansas USA"},{"name":"Arkansas Children's Research Institute  Little Rock Arkansas 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