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Recent works showed that conditional deletion of Bmal1 in myeloid cells (Bmal1DMye), which disrupt the macrophage clock, accelerated death in sepsis induced by both CLP (Deng et al., 2018) o r L P S (Curtis et al., 2015) and abolished the daily differences in the mortality rate. Bmal1DMyemice developed higher pro-inflammatory (Curtis et al., 2015) a n d a n t i inflammatory responses (Deng et al., 2018). The interaction between the pathogen and the host immune system is very complex and comprises two stages: an early stage characterized by excessive inflammation and a late stage characterized by sustained immune suppression (van der Poll et al., 2017). Therefore, it is not surprising tofind that Bmal1 is related to pro-inflammatory and anti-inflammatory processes, which are both deregulated during sepsis. In contrast, daily differences after LPS inoculation were not abolished in Bmal1DMyemice maintained under a time-restricted feeding schedule (Geiger et al., 2021). This discrepancy could be due to the different kinetics observed in the sepsis-induced mortality between models since the survival time was shorter in the last mentioned study. In addition, it is possible that mice fed only during the night have more robust peripheral circadian rhythms that may compensate for the lack of Bmal1 in myeloid cells, similar to what happens with the rhythm of the respiratory exchange rate in the same work.

最近的研究表明，髓系细胞中Bmal1的条件性缺失(Bmal1^ΔMye)扰乱了巨噬细胞的时钟，加速了CLP或rLPS诱导的脓毒症死亡，并消除了死亡率的每日差异。Bmal1^ΔMye鼠有更高的促炎反应和致炎反应。病原体与宿主免疫系统之间的相互作用非常复杂，包括两个阶段：以过度炎症为特征的早期阶段和以持续免疫抑制为特征的晚期阶段。因此，发现Bmal1与促炎和抗炎过程有关也就不足为奇了，两者在脓毒症时都均失调。相反，在Bmal1^ΔMye鼠中，在有时间限制的喂养时，接种LPS后的每日差异并未消除。这种差异可能是由于两种模型中观察到的脓毒症诱导死亡的动力学不同所致，因为最后提到的研究中Bmal1^ΔMye鼠存活时间较短。此外，只在夜间喂养的小鼠可能有更强的外周昼夜节律，这可能会弥补髓系细胞中Bmal1的缺乏，类似于同一工作中呼吸交换率的节律所发生的情况。