Introduction: Burn injury often induces immunosuppression, which is characterized, in part, by impairment of interleukin-12 (IL-12) and Interferon gamma (IFN-γ) secretion. Soluble β-glucans enhance host resistance to a broad spectrum of microbial pathogens. The present study was designed to determine whether glucan would reverse burn-induced suppression of IL-12 and IFN-γ secretion in vivo. Methods: Balb/C mice (4 mice/group) received 25% full-thickness flame burns under general anesthesia. Sham-burned mice served as controls. All mice were immediately resuscitated with normal saline (4 ml/ mouse IP) or saline containing glucan (40 mg/kg). On days 2 and 5 after burns, mice were challenged with E. coli endotoxin (LPS, 4 mg/kg IP) and serum samples were harvested for analysis of IL-12 and IFNγ levels using ELISA. Results: Priming of sham mice with glucan increased IL-12 secretion by 30-50% compared to saline-treated sham mice on days 2 and 5 after burn injury (see figure). Burn injury suppressed IL-12 secretion by 50-70%, yet glucan therapy restored serum IL-12 levels to those observed in non-burned control mice. Glucan priming enhanced IFNγ secretion in sham mice by 50-90% compared to saline-treated controls 6 hours after LPS challenge. Thermal injury suppressed LPS-induced IFNγ secretion by 50-60%. Treatment of burned mice with glucan restored LPS-induced IFNγ levels to those observed in non-burned controls. Conclusions: Thermal injury results in suppression of both IL-12 and IFNγ secretion. Treatment of thermally injured mice with glucan restores IL-12 and IFNγ levels to those observed in non-burned mice. Glucan may serve as an adjunctive immunomodulator to prevent burn-induced immunosuppression.
|Original language||English (US)|
|Journal||Critical care medicine|
|Issue number||12 SUPPL.|
|State||Published - Dec 1 1999|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine