Department of Intensive Care, Amsterdam University Medical Centers, location Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
Laboratory of Experimental Intensive Care and Anesthesiology, Amsterdam University Medical Centers, location Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
J Cell Mol Med. 2022 Apr;26(7):1896-1904. doi: 10.1111/jcmm.17156. Epub 2022 Mar 1.
The pathophysiology of hypothermia during sepsis is unclear. Using genomic profiling of blood leukocytes, we aimed to determine if hypothermia is associated with a different gene expression profile compared to fever during sepsis. Patients with sepsis and either hypothermia or fever within 24 hours after ICU admission were included in the study (n = 168). Hypothermia was defined as body temperature below 36 °C. Fever was defined as body temperature equal to or above 38.3°C. We compared blood gene expression (whole-genome transcriptome in leukocytes) in hypothermic septic compared to febrile septic patients in an unmatched analysis and matched for APACHE IV score and the presence of shock. In total, 67 septic patients were hypothermic and 101 patients were febrile. Hypothermia was associated with a distinct gene expression profile in both unmatched and matched analyses. There were significant differences related to the up- and downregulation of canonical signalling pathways. In the matched analysis, the top upregulated gene was cold-inducible mRNA binding protein (CIRBP) which plays a role in cold-induced suppression of cell proliferation. In addition, we found three signalling pathways significantly upregulated in hypothermic patients compared to febrile patients; tryptophan degradation X, phenylalanine degradation IV and putrescine degradation III. In conclusion, there are distinct signalling pathways and genes associated with hypothermia, including tryptophan degradation and CIRBP expression, providing a possible link to the modulation of body temperature and early immunosuppression. Future studies may focus on the canonical signalling pathways presented in this paper to further investigate spontaneous hypothermia in sepsis.
脓毒症患者低温发生的病理生理学机制尚不清楚。本研究采用血液白细胞基因组谱分析,旨在确定与脓毒症发热患者相比,低温患者是否存在不同的基因表达谱。研究纳入了入住 ICU 24 小时内出现低温或发热的脓毒症患者(n=168)。低温定义为体温低于 36°C,发热定义为体温等于或高于 38.3°C。我们在未匹配分析和匹配 APACHE IV 评分及休克存在情况下,比较了低温脓毒症患者与发热脓毒症患者的血液基因表达(白细胞全基因组转录组)。共有 67 例脓毒症患者为低温,101 例患者为发热。未匹配和匹配分析均显示低温与独特的基因表达谱相关。存在与经典信号通路上调和下调相关的显著差异。在匹配分析中,上调最明显的基因是冷诱导 RNA 结合蛋白(CIRBP),其在冷诱导抑制细胞增殖中发挥作用。此外,与发热患者相比,我们还发现低温患者中有 3 条信号通路显著上调,即色氨酸降解 X、苯丙氨酸降解 IV 和腐胺降解 III。总之,低温与特定的信号通路和基因相关,包括色氨酸降解和 CIRBP 表达,这可能与体温调节和早期免疫抑制有关。未来的研究可能集中在本文提出的经典信号通路上,以进一步研究脓毒症中自发性低温的机制。