{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T15:01:50Z","timestamp":1772895710975,"version":"3.50.1"},"reference-count":50,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","license":[{"start":{"date-parts":[[2002,4,1]],"date-time":"2002-04-01T00:00:00Z","timestamp":1017619200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"},{"start":{"date-parts":[[2003,12,30]],"date-time":"2003-12-30T00:00:00Z","timestamp":1072742400000},"content-version":"vor","delay-in-days":638,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"crossref","award":["DK 52232"],"award-info":[{"award-number":["DK 52232"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2002,4]]},"abstract":"<jats:sec>\n            <jats:title\/>\n            <jats:p>Endotoxin has been identified as a principal mediator of sepsis, often with resulting multiple organ failure. Although interferon \u03b3 (IFN-\u03b3) has a central role in controlling bacterial infection through the activation of macrophages and T lymphocytes, it can also enhance the harmful effects of the inflammatory response. To examine the role of IFN-\u03b3 in lipopolysaccharide (LPS)-induced injury, we administered LPS (20 or 800 \u03bcg\/mouse) alone or as low-dose LPS (20 \u03bcg\/mouse) 7 days after heat-killed <jats:italic toggle=\"yes\">Propionibacterium acnes<\/jats:italic> (<jats:italic toggle=\"yes\">P. acnes<\/jats:italic>) injection into wild-type C57BL\/6 (B6) mice or IFN-\u03b3-deficient (GKO) mice (B6 background). Although low-dose (20 \u03bcg) LPS alone had no effect on survival, the administration of 800 \u03bcg LPS alone resulted in 100% mortality in both B6 and GKO mice without significant hepatic mononuclear cellular infiltration or differences in elevated plasma tumor necrosis factor \u03b1 (TNF-\u03b1), interleukin 6 (IL-6), and IL-12 levels. In contrast, mortality after low-dose (20 \u03bcg) LPS challenge in <jats:italic toggle=\"yes\">P. acnes<\/jats:italic>-primed B6 mice was 100%, but 0% in GKO mice. <jats:italic toggle=\"yes\">In vivo<\/jats:italic> plasma cytokine (IFN-\u03b3, TNF-\u03b1, IL-6, and IL-12) levels and <jats:italic toggle=\"yes\">in vitro<\/jats:italic> cytokine production by hepatic mononuclear cells were significantly higher in B6 mice compared with GKO mice. Associated hepatic mononuclear cellular infiltration, multifocal liver necrosis, hepatomegaly, and splenomegaly were found in B6 mice, but not in GKO mice. Finally, the anti-inflammatory NK1.1+CD4+ cell proportion of hepatic infiltrating mononuclear cell numbers 7 days after <jats:italic toggle=\"yes\">P. acnes<\/jats:italic> administration was significantly reduced in B6 compared with GKO mice, whereas the proportion of inflammatory NK1.1+CD4\u2212 cells was increased. In conclusion, these data suggest that IFN-\u03b3 mediates <jats:italic toggle=\"yes\">P. acnes<\/jats:italic>-primed low-dose LPS injury through the hepatic infiltration of mononuclear cells and the subsequent elevation of inflammatory cytokines after LPS challenge, whereas the lethal effects of high-dose LPS alone does not depend on the presence of IFN-\u03b3.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1053\/jhep.2002.32484","type":"journal-article","created":{"date-parts":[[2002,8,25]],"date-time":"2002-08-25T03:46:10Z","timestamp":1030247170000},"page":"805-814","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":28,"title":["The resistance of P. acnes -primed interferon \u03b3-deficient mice to low-dose lipopolysaccharide-induced acute liver injury"],"prefix":"10.1097","volume":"35","author":[{"given":"Yoshiaki","family":"Shimizu","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie A.","family":"Margenthaler","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Keith","family":"Landeros","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naoki","family":"Otomo","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gerard","family":"Doherty","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wayne M.","family":"Flye","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"issue":"Suppl 1","key":"10.1053\/jhep.2002.32484-BIB1|cit1","doi-asserted-by":"crossref","first-page":"S28","DOI":"10.1136\/gut.35.1_Suppl.S28","article-title":"Clinical significance of translocation","volume":"35","author":"Van Leeuwen","year":"1994","journal-title":"Gut"},{"key":"10.1053\/jhep.2002.32484-BIB2|cit2","doi-asserted-by":"crossref","first-page":"191","DOI":"10.1002\/hep.1840160130","article-title":"Lipopolysaccharide treatment of rats alters antigen expression and oxidative metabolism in hepatic macrophages and endothelial cells","volume":"16","author":"McCloskey","year":"1992","journal-title":"Hepatology"},{"key":"10.1053\/jhep.2002.32484-BIB3|cit3","doi-asserted-by":"crossref","first-page":"456","DOI":"10.1016\/0016-5085(89)91571-0","article-title":"Clearance of gut-derived endotoxins by the liver. 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