TY - JOUR
T1 - Inhibition of induction of natural killer activity in mice by general anesthesia (Avertin)
T2 - Role of interferon
AU - Markovic, Svetomir N.
AU - Murasko, Donna M.
N1 - Funding Information:
work was supported by CA43386.
PY - 1991/8
Y1 - 1991/8
N2 - We have previously reported that general anesthesia (Avertin) inhibits the induction of natural killer (NK) cell activity following administration of Poly I:C in vivo. Since Poly I:C has been shown to increase NK activity through the induction of interferon (IFN), the current study examines the role of IFN in this inhibition. The data suggest that (i) anesthesia does not effect the ability of Poly I:C to induce endogenous IFN synthesis (serum IFN levels are unaltered by anesthesia) and (ii) anesthesia is capable of inhibiting stimulation of NK activity induced directly by treatment with IFN either in vivo or in vitro. The duration of the former effect was at least 10 days, with complete recovery by Day 14 after anesthesia. Interestingly, NK activity stimulated by IFN prior to anesthesia was not significantly altered. In view of the increasingly evident role of NK cells in anti-tumor and anti-infectious host defenses, their inertness to stimulation in the postanesthesia period may be a significant contributing factor to the clinically observed postoperative morbidity. Thus, preanesthesia stimulation of NK activity with IFN may be of therapeutic value.
AB - We have previously reported that general anesthesia (Avertin) inhibits the induction of natural killer (NK) cell activity following administration of Poly I:C in vivo. Since Poly I:C has been shown to increase NK activity through the induction of interferon (IFN), the current study examines the role of IFN in this inhibition. The data suggest that (i) anesthesia does not effect the ability of Poly I:C to induce endogenous IFN synthesis (serum IFN levels are unaltered by anesthesia) and (ii) anesthesia is capable of inhibiting stimulation of NK activity induced directly by treatment with IFN either in vivo or in vitro. The duration of the former effect was at least 10 days, with complete recovery by Day 14 after anesthesia. Interestingly, NK activity stimulated by IFN prior to anesthesia was not significantly altered. In view of the increasingly evident role of NK cells in anti-tumor and anti-infectious host defenses, their inertness to stimulation in the postanesthesia period may be a significant contributing factor to the clinically observed postoperative morbidity. Thus, preanesthesia stimulation of NK activity with IFN may be of therapeutic value.
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U2 - 10.1016/0090-1229(91)90062-F
DO - 10.1016/0090-1229(91)90062-F
M3 - Article
C2 - 1712686
AN - SCOPUS:0025873175
SN - 0090-1229
VL - 60
SP - 181
EP - 189
JO - Clinical Immunology and Immunopathology
JF - Clinical Immunology and Immunopathology
IS - 2
ER -