Kiank Cornelia, Koerner Pia, Kessler Wolfram, Traeger Tobias, Maier Stefan, Heidecke Claus-Dieter, Schuett Christine
Departments of Immunology, University of Greifswald, Greifswald, Germany.
Crit Care Med. 2007 Oct;35(10):2352-8. doi: 10.1097/01.ccm.0000282078.80187.7f.
In this study, we analyzed seasonal variations of immunoreactivity using a model of septic shock and a model of immunosuppression induced by chronic stress in mice.
Retrospective comparative study using animals of experiments performed between 2001 and 2006 to identify seasonal variations in inflammatory responsiveness of mice.
University-based research laboratory.
C57Bl/6 mice and BALB/c mice.
For analyzing septic shock, we used the hyperinflammatory model of colon ascendens stent peritonitis. Immunosuppression was induced by 4.5 days of intermittent combined acoustic and restraint stress.
We show that mice kept with 12:12-hr light/dark rhythm had an enhanced risk to die of experimentally-induced hyperinflammatory peritonitis performed in summer or autumn compared with the other seasons. This finding was associated with an exaggerated proinflammatory response of C57Bl/6 mice in summer or autumn compared with moderate inflammatory reactivity in winter and spring. Consistent with these results, we report that the severity of a stress-induced immunosuppression is less pronounced in BALB/c mice that were exposed to chronic psychological stress in the summer compared with exposure in winter. Coping with chronic psychological stress of these animals was correlated with less pronounced corticosterone release, less severe lymphocytopenia, and a lower ex vivo inducibility of interleukin-10, thereby attenuating a stress-mediated immunosuppressive state. Mice subjected to chronic stress in the summer season showed increased coping compared with mice that were stressed in the winter season.
Our results suggest that seasonal changes of the host's hypothalamus-pituitary-adrenal axis response influence the risk of infection and the susceptibility to stress, which interferes with the outcome after infection.
在本研究中,我们使用脓毒症休克模型和慢性应激诱导的免疫抑制模型分析了小鼠免疫反应性的季节性变化。
回顾性比较研究,使用2001年至2006年间进行实验的动物来确定小鼠炎症反应性的季节性变化。
大学研究实验室。
C57Bl/6小鼠和BALB/c小鼠。
为分析脓毒症休克,我们使用了升结肠支架腹膜炎的高炎症模型。通过4.5天的间歇性声音和束缚联合应激诱导免疫抑制。
我们发现,与其他季节相比,保持12小时光照/12小时黑暗节律的小鼠在夏季或秋季进行实验性诱导的高炎症性腹膜炎时死亡风险增加。这一发现与C57Bl/6小鼠在夏季或秋季的促炎反应过度有关,而在冬季和春季则为中度炎症反应。与这些结果一致,我们报告说,与冬季相比,夏季暴露于慢性心理应激的BALB/c小鼠中,应激诱导的免疫抑制严重程度较轻。这些动物应对慢性心理应激与皮质酮释放不那么明显、淋巴细胞减少不那么严重以及白细胞介素-10的体外诱导性较低相关,从而减轻了应激介导的免疫抑制状态。与冬季应激的小鼠相比,夏季遭受慢性应激的小鼠表现出更强的应对能力。
我们的结果表明,宿主下丘脑-垂体-肾上腺轴反应的季节性变化会影响感染风险和对应激的易感性,进而干扰感染后的结局。