Toth L A
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, USA.
J Interferon Cytokine Res. 1996 Dec;16(12):1065-72. doi: 10.1089/jir.1996.16.1065.
Increased slow-wave sleep accompanies influenza infection in C57BL/6 mice but not BALB/c mice. These strains of mice possess different alleles of the genetic lucus If-1, which codes for high (If-1h; C57BL/6) and low (If-1(1); BALB/c) production of interferon (IFN), a putative sleep-inducing cytokine. To evaluate the contribution of the If-1 gene to differences in murine sleep propensity, sleep patterns were evaluated in mice treated with the IFN inducers polyinosinic:polycytidilic acid (pIC) or Newcastle disease virus (NDV), with influenza virus, or with murine interferon (IFN-alpha) or IFN-alpha/beta. As compared with baseline values, C57BL/6 mice exhibited increased slow-wave sleep after all three challenges, but BALB/c mice did not. Congenic B6.C-H28c mice, which bear the BALB/c allele for low IFN production on the C57BL/6 genetic background, showed enhanced slow-wave sleep after influenza infection but not after NDV. Exogenous IFN did not enhance slow-wave sleep in either C57BL/6 or BALB/c mice. These data suggest that the If-1 allele may influence the somnogenic responsiveness of mice under some conditions but that additional mechanisms may contribute to sleep enhancement during infectious disease.
在C57BL/6小鼠感染流感时慢波睡眠会增加,但BALB/c小鼠不会。这两种品系的小鼠具有不同的If-1基因座等位基因,该基因座编码干扰素(IFN)的高产量(If-1h;C57BL/6)和低产量(If-1l;BALB/c),干扰素是一种假定的诱导睡眠的细胞因子。为了评估If-1基因对小鼠睡眠倾向差异的影响,对用IFN诱导剂多聚肌苷酸:多聚胞苷酸(pIC)或新城疫病毒(NDV)、流感病毒、小鼠干扰素(IFN-α)或IFN-α/β处理的小鼠的睡眠模式进行了评估。与基线值相比,C57BL/6小鼠在所有三种刺激后慢波睡眠均增加,但BALB/c小鼠没有。在C57BL/6遗传背景上携带低IFN产量的BALB/c等位基因的同源B6.C-H28c小鼠,在感染流感后慢波睡眠增强,但在感染NDV后没有。外源性IFN在C57BL/6或BALB/c小鼠中均未增强慢波睡眠。这些数据表明,If-1等位基因可能在某些条件下影响小鼠的促睡眠反应,但在传染病期间睡眠增强可能还有其他机制。