Renegar K B, Floyd R, Krueger J M
Department of Physiology and Biophysics, University of Tennessee, Memphis, USA.
Sleep. 1998;21(1):19-24.
Intra-pulmonary protection against influenza virus in immune mice, largely dependent upon serum lgG, is reported to be suppressed by 7 hours of sleep deprivation following viral challenge. This implies that sleep deprivation may accelerate the catabolism of influenza-specific antibodies. To determine the effects of sleep deprivation on the catabolism of serum antibodies, BALB/c mice were passively immunized intravenously with lgG anti-influenza monoclonalantibodies and catabolism kinetics monitored for 6 days. Mice were then sleep-deprived for either 9 hours (one episode) or for 9 hours followed by 6 hours on the consecutive day (two episodes) and the serum titer of influenza-specific monoclonal antibodies monitored for an additional 8 days via ELISA. One episode of sleep-deprivation had only minor effects on lgG catabolism; however, two episodes of sleep-deprivation caused significant changes in the kinetics of lgG catabolism, resulting in elevated lgG levels (p = 0.02) for 2 days post-sleep deprivation. Elevation of serum influenza-specific lgG (p = 0.005) was also seen in actively immune mice following two episodes of sleep-deprivation. Serum chemistries ruled out dehydration as a cause of the increased antibody levels; however, some anomalies were noted: total protein and albumin were elevated, although not significantly, and P and Ca were decreased. Thus, our data do not support the hypothesis that sleep-deprivation lowers existing serum antibody titers by accelerating antibody catabolism.
