Abstract
The mechanism by which EtOH potentiates post burn pathogenesis remains unknown. We have shown that EtOH intoxication prior to burn injury potentiates the suppression of mesenteric lymph node (MLN) T cell IL‐2/IFN‐γ and enhances bacterial translocation. The suppression in T cell was accompanied with a decrease in p38 and ERK activation. Since we also found a decrease in IL‐12, this study examined whether IL‐12 restitution restores T cell IL‐2/IFN‐γ following EtOH and burn injury and whether p38/ERK pathway is involved in IL‐12 restoration of IL‐2/IFN‐γ. Male rats (250g) were gavaged with 5 ml of 20% EtOH 4h prior to ~12.5% total body surface area burn or sham injury. Rats were sacrificed on day one after injury. MLN T cells were isolated, stimulated with anti‐CD3 in the absence or presence of recombinant (r) IL‐12 (10ng/ml) for 5 min and lysed for p38 and ERK1/2 measurements. In some experiments, T cells were cultured for 48h with or without the inhibitors of p38 (10μM SB203580) or ERK (50μM PD98059). Results indicate that the incubation of T cells with rIL‐12 prevents the suppression of T cell IL‐2/IFN‐γ following EtOH and burn injury. Furthermore, IL‐12 normalizes both p38 and ERK activation in T cells, but results obtained using p38 and ERK inhibitors indicate that the restoration of ERK and not p38 is critical to IL‐12‐mediated restoration of T cell IL‐2/IFN‐γ production following EtOH and burn injury. (R01AA015731–01A2)
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