{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T13:15:02Z","timestamp":1790082902562,"version":"4.0.1"},"reference-count":80,"publisher":"Oxford University Press (OUP)","issue":"7","license":[{"start":{"date-parts":[[2025,5,12]],"date-time":"2025-05-12T00:00:00Z","timestamp":1747008000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01AA028763"],"award-info":[{"award-number":["R01AA028763"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01HL155064"],"award-info":[{"award-number":["R01HL155064"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01HL166544"],"award-info":[{"award-number":["R01HL166544"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Alcohol use disorder increases sepsis mortality. Acute ethanol exposure impairs pathogen clearance in the macrophages via dampened glycolysis and phagocytosis, exaggerates oxidative stress, and regulates the function of the hypoxia-regulating factor 1\u03b1 (HIF-1\u03b1), a master regulator of glycolysis. Decreased expression of the platelet isoform of phosphofructokinase (PFKP), a key glycolytic enzyme, in ethanol-exposed macrophages, is reported. However, transcriptional regulation of PFKP with ethanol exposure is unclear. We hypothesized that acute ethanol exposure\u2013induced oxidative stress dampens macrophage phagocytosis and glycolysis via the HIF-1\u03b1-PFKP axis. In ethanol-exposed mouse bone marrow\u2013derived macrophages with lipopolysaccharide stimulation, we studied (i) reactive oxygen species (ROS), phagocytosis, glycolysis, PFKP, and HIF-1\u03b1 expressions \u00b1 ethanol exposure; (ii) the role of HIF-1\u03b1 in transcriptionally controlling PFKP messenger RNA by chromatin immunoprecipitation\u2013quantitative polymerase chain reaction technique; and (iii) the effect of mitoquinol (MitoQ), a mitochondria-specific antioxidant, on HIF-1\u03b1 function, glycolysis, phagocytosis, and pathogen clearance in ethanol-exposed macrophages. Last, we examined the effect of MitoQ on 7-d survival in alcohol vs. vehicle-drinking mice with cecal slurry\u2013induced sepsis. In ethanol-exposed and lipopolysaccharide\u2013stimulated macrophages, we found that (i) excessive total and mitochondrial ROS production and dampened phagocytosis, glycolysis, and PFKP expression; (ii) dysfunctional HIF-1\u03b1 downregulates PFKP transcription; (iii) MitoQ restrains ROS production, restores HIF-1\u03b1 function, and improves glycolysis and phagocytosis via preserved PFKP messenger RNA and protein expression; and (iv) MitoQ treatment improves survival and pathogen clearance in ethanol with sepsis mice. In conclusion, we found that the HIF-1\u03b1-PFKP axis regulates glycolysis and phagocytosis in ethanol-exposed macrophages and is a potential therapeutic target in ethanol with sepsis.<\/jats:p>","DOI":"10.1093\/jimmun\/vkaf078","type":"journal-article","created":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T00:34:23Z","timestamp":1747096463000},"page":"1754-1772","source":"Crossref","is-referenced-by-count":6,"title":["Mitoquinol improves phagocytosis and glycolysis in ethanol-exposed macrophages via HIF-1\u03b1-PFKP axis"],"prefix":"10.1093","volume":"214","author":[{"given":"Bishnu D","family":"Pant","sequence":"first","affiliation":[{"name":"Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0063-5025","authenticated-orcid":false,"given":"Akash","family":"Ahuja","sequence":"additional","affiliation":[{"name":"Inflammation and 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