{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,29]],"date-time":"2026-01-29T04:55:53Z","timestamp":1769662553093,"version":"3.49.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2009,9,1]],"date-time":"2009-09-01T00:00:00Z","timestamp":1251763200000},"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":[[2009,9,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Previous studies from our laboratory have shown that acute alcohol\/ethanol (EtOH) intoxication combined with burn injury suppresses T cell IL-2 and IFN-\u03b3 production by inhibiting p38 and ERK activation. Because IL-12 plays a major role in Th1 differentiation and IFN-\u03b3 production, we examined whether diminished IL-2 and IFN-\u03b3 production after EtOH plus burn injury resulted from a decrease in IL-12. Furthermore, we investigated whether IL-12 utilizes the p38\/ERK pathway to modulate T cell IL-2 and IFN-\u03b3 production after EtOH and burn injury. Male rats (\u223c250 g) were gavaged with 5 ml of 20% EtOH 4 h before \u223c12.5% total body surface area burn or sham injury. Rats were sacrificed on day 1 after injury, and mesenteric lymph node T cells were isolated. T cells were stimulated with anti-CD3 in the absence or presence of rIL-12 (10 ng\/ml) for 5 min and lysed. Lysates were analyzed for p38\/ERK protein and phosphorylation levels using specific Abs and Western blot. In some experiments, T cells were cultured for 48 h with or without the inhibitors of p38 (10 \u03bcM SB203580\/SB202190) or ERK (50 \u03bcM PD98059) to delineate the role of p38 and ERK in IL-12-mediated restoration of IL-2 and IFN-\u03b3. Our findings indicate that IL-12 normalizes both p38 and ERK activation in T cells, but the results obtained using p38 and ERK inhibitors indicate that the restoration of ERK plays a predominant role in IL-12-mediated restoration of T cell IL-2 and IFN-\u03b3 production after EtOH and burn injury.<\/jats:p>","DOI":"10.4049\/jimmunol.0804103","type":"journal-article","created":{"date-parts":[[2009,8,26]],"date-time":"2009-08-26T22:24:00Z","timestamp":1251325440000},"page":"3955-3962","source":"Crossref","is-referenced-by-count":20,"title":["ERK and Not p38 Pathway Is Required for IL-12 Restoration of T Cell IL-2 and IFN-\u03b3 in a Rodent Model of Alcohol Intoxication and Burn Injury"],"prefix":"10.1093","volume":"183","author":[{"given":"Xiaoling","family":"Li","sequence":"first","affiliation":[{"name":"Burn and Shock Trauma Institute and Alcohol Research Program, Department of Surgery, Loyola University Chicago Medical Center , Maywood, IL 60153"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Irshad H","family":"Chaudry","sequence":"additional","affiliation":[{"name":"Center for Surgical Research and Departments of Surgery, University of Alabama , Birmingham, AL 35226"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mashkoor A","family":"Choudhry","sequence":"additional","affiliation":[{"name":"Burn and Shock Trauma Institute and Alcohol Research Program, Department of Surgery, Loyola University Chicago Medical Center , Maywood, IL 60153"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2009,9,15]]},"reference":[{"key":"2026012811234118800_R1","first-page":"15","article-title":"Alcohol abuse: a major contributing factor to post-burn\/trauma immune complications. 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