Inhibition of induction of natural killer activity in mice by general anesthesia (Avertin): Role of interferon

Svetomir Nenad Markovic, Donna M. Murasko

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11 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)181-189
Number of pages9
JournalClinical Immunology and Immunopathology
Volume60
Issue number2
DOIs
StatePublished - 1991
Externally publishedYes

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General Anesthesia
Interferons
Anesthesia
Poly I-C
Natural Killer Cells
Population Growth
tribromoethanol
Morbidity
Serum
Neoplasms

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Pathology and Forensic Medicine

Cite this

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title = "Inhibition of induction of natural killer activity in mice by general anesthesia (Avertin): Role of interferon",
abstract = "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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AU - Markovic, Svetomir Nenad

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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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