{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:07:16Z","timestamp":1791184036418,"version":"4.1.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2002,3,1]],"date-time":"2002-03-01T00:00:00Z","timestamp":1014940800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2002,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Cellular responses to endotoxins are enhanced markedly by LPS-binding protein (LBP). Furthermore, it has been demonstrated that endotoxins and proinflammatory cytokines such as TNF-\u03b1 participate in early alcohol-induced liver injury. Therefore, in this study, a long-term intragastric ethanol feeding model was used to test the hypothesis that LBP is involved in alcoholic hepatitis by comparing LBP knockout and wild-type mice. Two-month-old female mice were fed a high-fat liquid diet with either ethanol or isocaloric maltose-dextrin as control continuously for 4 wk. There was no difference in mean urine alcohol concentrations between the groups fed ethanol. Dietary alcohol significantly increased liver to body weight ratios and serum alanine aminotransferase levels in wild-type mice (189 \u00b1 31 U\/L) over high-fat controls (24 \u00b1 7 U\/L), effects which were blunted significantly in LBP knockout mice (60 \u00b1 17 U\/L). Although no significant pathological changes were observed in high-fat controls, 4 wk of dietary ethanol caused steatosis, mild inflammation, and focal necrosis in wild-type animals as expected (pathology score, 5.9 \u00b1 0.5). These pathological changes were reduced significantly in LBP knockout mice fed ethanol (score, 2.6 \u00b1 0.5). Endotoxin levels in the portal vein were increased significantly after 4 wk in both groups fed ethanol. Moreover, ethanol increased TNF-\u03b1 mRNA expression in wild-type, but not in LBP knockout mice. These data are consistent with the hypothesis that LBP plays an important role in early alcohol-induced liver injury by enhancing LPS-induced signal transduction, most likely in Kupffer cells.<\/jats:p>","DOI":"10.4049\/jimmunol.168.6.2963","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T00:31:13Z","timestamp":1398040273000},"page":"2963-2969","source":"Crossref","is-referenced-by-count":153,"title":["Role of Lipopolysaccharide-Binding Protein in Early Alcohol-Induced Liver Injury in Mice"],"prefix":"10.1093","volume":"168","author":[{"given":"Takehiko","family":"Uesugi","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Froh","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gavin E","family":"Arteel","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Blair U","family":"Bradford","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael D","family":"Wheeler","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erwin","family":"Ga\u0308bele","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fuyumi","family":"Isayama","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald G","family":"Thurman","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Laboratory of Hepatobiology and Toxicology, University of North Carolina , Chapel Hill, NC 27599"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,3,15]]},"reference":[{"key":"2025032712351399300_R1","first-page":"2652","volume-title":"FASEB J.","year":"1991"},{"key":"2025032712351399300_R2","first-page":"S205","volume-title":"Clin. 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