Cell resilience in species life spans: a link to inflammation?
Cell resilience in species life spans: a link to inflammation?
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DOI：
10.1111/j.1474-9726.2010.00578.x
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发表时间：
2010-08-01
期刊：
影响因子：
7.8
通讯作者：
de Magalhaes, Joao P.
中科院分区：
文献类型：
--
作者：
Finch, Caleb E.;Morgan, Todd E.;de Magalhaes, Joao P.
物种寿命的差异归因于细胞在各种压力下的存活，在这里被称为“细胞耐受性”。在原代成纤维细胞培养中，细胞在暴露于自由基、低血糖、高热和各种毒素的过程中的恢复力已经显示出与鸟类和哺乳动物的物种特征寿命大体一致的相关性。然而，成纤维细胞培养物中细胞弹性与不同物种寿命的机制联系知之甚少。我们提出，某些实验应激相关的体细胞损伤在体内先天免疫的炎症反应，特别是，抵抗活性氧（ROS），低葡萄糖，和高热。根据这一假说，体细胞弹性决定了物种在自然环境中反复感染和创伤性损伤期间的寿命差异。感染和损伤使局部成纤维细胞和其他细胞暴露于巨噬细胞产生的ROS和局部温度升高。全身性的，急性期免疫反应引起低血糖和高热。我们认为，细胞对炎症引起的躯体压力源的恢复力在长寿的进化中很重要，并且长寿的物种特别对免疫相关的压力源更具抵抗力。这一假说进一步明确了柯克伍德的可抛弃的索马理论。我们建议扩大电池的压力和标记物用于比较研究，以额外的细胞类型和其他参数相关的主机防御和他们的生态特性。
P>Species differences in life span have been attributed to cellular survival during various stressors, designated here as 'cell resilience'. In primary fibroblast cultures, cell resilience during exposure to free radicals, hypoglycemia, hyperthermia, and various toxins has shown generally consistent correlations with the species characteristic life spans of birds and mammals. However, the mechanistic links of cell resilience in fibroblast cultures to different species life spans are poorly understood. We propose that certain experimental stressors are relevant to somatic damage in vivo during inflammatory responses of innate immunity, particularly, resistance to reactive oxygen species (ROS), low glucose, and hyperthermia. According to this hypothesis, somatic cell resilience determines species differences in longevity during repeated infections and traumatic injuries in the natural environment. Infections and injury expose local fibroblasts and other cells to ROS generated by macrophages and to local temperature elevations. Systemically, acute phase immune reactions cause hypoglycemia and hyperthermia. We propose that cell resilience to somatic stressors incurred in inflammation is important in the evolution of longevity and that longer-lived species are specifically more resistant to immune-related stressors. This hypothesis further specifies Kirkwood's disposable soma theory. We suggest expanding the battery of stressors and markers used for comparative studies to additional cell types and additional parameters relevant to host defense and to their ecological specificities.