TY - JOUR
T1 - Acute alcohol intoxication potentiates neutrophil-mediated intestinal tissue damage after burn injury
AU - Li, Xiaoling
AU - Schwacha, Martin G.
AU - Chaudry, Irshad H.
AU - Choudhry, Mashkoor A.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2008/3
Y1 - 2008/3
N2 - This study examined whether acute alcohol (EtOH) intoxication before burn injury potentiates postburn intestinal tissue damage and whether neutrophils have any role in the damage under those conditions. Male rats (∼250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL or with saline and received either approximately 12.5% or approximately 25% total body surface area (TBSA) burn or sham injury. Rats were killed at 4 or 24 h after injury, and various parameters were measured. As compared with sham animals, burn injury alone (regardless of size) resulted in a significant increase in intestinal tissue myeloperoxidase (MPO; an index of neutrophil infiltration) activity and IL-18 levels 4 h after injury. Furthermore, rats receiving 25% TBSA, but not 12.5%, burn exhibited intestine edema. The IL-18 and MPO activity were normalized at 24 h after injury in rats receiving 12.5% TBSA burn, whereas these parameters remained elevated at 24 h in rats with 25% burn. The presence of EtOH in rats at the time of burn injury exacerbated the levels of IL-18, MPO activity, and edema at 4 and 24 h after burn injury. Treatment of rats with anti-IL-18 antibodies or with antineutrophil antiserum prevented the increase in the above parameters after EtOH and burn injury, except that the depletion of neutrophils did not prevent the IL-18 increase. In summary, these findings suggest that acute EtOH intoxication exacerbates postburn intestinal tissue damage after burn injury, and that it is, in part, neutrophil mediated.
AB - This study examined whether acute alcohol (EtOH) intoxication before burn injury potentiates postburn intestinal tissue damage and whether neutrophils have any role in the damage under those conditions. Male rats (∼250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL or with saline and received either approximately 12.5% or approximately 25% total body surface area (TBSA) burn or sham injury. Rats were killed at 4 or 24 h after injury, and various parameters were measured. As compared with sham animals, burn injury alone (regardless of size) resulted in a significant increase in intestinal tissue myeloperoxidase (MPO; an index of neutrophil infiltration) activity and IL-18 levels 4 h after injury. Furthermore, rats receiving 25% TBSA, but not 12.5%, burn exhibited intestine edema. The IL-18 and MPO activity were normalized at 24 h after injury in rats receiving 12.5% TBSA burn, whereas these parameters remained elevated at 24 h in rats with 25% burn. The presence of EtOH in rats at the time of burn injury exacerbated the levels of IL-18, MPO activity, and edema at 4 and 24 h after burn injury. Treatment of rats with anti-IL-18 antibodies or with antineutrophil antiserum prevented the increase in the above parameters after EtOH and burn injury, except that the depletion of neutrophils did not prevent the IL-18 increase. In summary, these findings suggest that acute EtOH intoxication exacerbates postburn intestinal tissue damage after burn injury, and that it is, in part, neutrophil mediated.
KW - Cytokines
KW - Ethanol
KW - Inflammation
KW - Intestine permeability
KW - Myeloperoxidase
KW - Trauma
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U2 - 10.1097/SHK.0b013e31815abe80
DO - 10.1097/SHK.0b013e31815abe80
M3 - Article
C2 - 18000475
AN - SCOPUS:39449083329
VL - 29
SP - 377
EP - 383
JO - Shock
JF - Shock
SN - 1073-2322
IS - 3
ER -