Renegar K B, Floyd R A, Krueger J M
Department of Surgery, University of Tennessee, Memphis, USA.
Sleep. 1998 May 1;21(3):241-8.
Sleep has been proposed as an innate host defense, exerting effects on both specific and nonspecific immunity. In one of the more striking papers dealing with the effects of sleep on specific immunity, Brown et al (Reg. Immunol. 1989; 2: 321-325) reported that depriving influenza virus-immune mice of sleep for 7 hours following total respiratory tract viral challenge abrogated anti-viral immunity within the lungs and lowered the level of anti-influenza antibody in lung homogenates. In the solidly-immune convalescent mouse, nasobronchial immunity to influenza virus has been shown to be due to secretory IgA (S-IgA) within the mucosal mucocilliary blanket, while serum IgG has been shown to mediate protection within the lung parenchyma. In this study we attempted to duplicate the work of Brown et al in solidly immune mice. We were unable to abrogate mucosal anti-influenza viral immunity with a single post-viral-challenge sleep-deprivation episode, nor were we able to depress this immunity with one pre- and two post-challenge sleep-deprivation episodes in young adult or old mice, or with two pre-challenge sleep-deprivation episodes in old mice. Sleep deprivation did not depress the level of serum influenza-specific IgG antibodies, and resulted in increased influenza-specific serum IgG compared with normally sleeping mice in aged immune mice boosted 3 weeks before challenge and sleep deprived once before and twice after challenge (p = 0.005). No differences in anti-viral respiratory immunity were apparent between young and old mice. We conclude that short-term sleep deprivation has minimal effects on pre-existing mucosal and humoral immunity in either the young adult or the senescent mouse.
睡眠被认为是一种先天性的宿主防御机制，对特异性免疫和非特异性免疫均有影响。在一篇关于睡眠对特异性免疫影响的更引人注目的论文中，布朗等人（《调节免疫学》，1989年；2：321 - 325）报告称，在全呼吸道病毒攻击后，剥夺感染流感病毒的免疫小鼠7小时睡眠会消除肺部的抗病毒免疫力，并降低肺匀浆中抗流感抗体的水平。在完全免疫的恢复期小鼠中，鼻支气管对流感病毒的免疫已被证明是由于黏膜黏液纤毛覆盖层中的分泌型IgA（S - IgA），而血清IgG已被证明在肺实质内介导保护作用。在本研究中，我们试图在完全免疫的小鼠中重复布朗等人的工作。我们无法通过单次病毒攻击后的睡眠剥夺来消除黏膜抗流感病毒免疫力，在年轻成年或老年小鼠中，也无法通过一次攻击前和两次攻击后的睡眠剥夺，或在老年小鼠中通过两次攻击前的睡眠剥夺来降低这种免疫力。睡眠剥夺并未降低血清流感特异性IgG抗体水平，在攻击前3周进行免疫增强、攻击前一次和攻击后两次进行睡眠剥夺的老年免疫小鼠中，与正常睡眠小鼠相比，睡眠剥夺导致流感特异性血清IgG增加（p = 0.005）。年轻和老年小鼠之间的抗病毒呼吸道免疫没有明显差异。我们得出结论：短期睡眠剥夺对年轻成年或老年小鼠预先存在的黏膜和体液免疫影响极小。
