Hypothermia increases interleukin-6 and interleukin-10 in juvenile endotoxemic mice.
Hypothermia increases interleukin-6 and interleukin-10 in juvenile endotoxemic mice.
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DOI：
10.1097/pcc.0b013e3181b01042
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发表时间：
2010-01
期刊：
影响因子：
--
通讯作者：
Fairchild KD
中科院分区：
文献类型：
--
作者：
Stewart CR;Landseadel JP;Gurka MJ;Fairchild KD
To develop a juvenile mouse model to establish effects of in vivo hypothermia on expression of the inflammation-modulating cytokines tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-10. Although induced hypothermia is neuroprotective in some patients, the mechanisms of protection are not well understood and concerns remain over potential detrimental effects, particularly in the setting of infection. We previously showed that in vitro hypothermia increases production of tumor necrosis factor-α and interleukin-1β in lipopolysaccharide-treated monocytes. Laboratory investigation. Research laboratory. Juvenile (4-wk) male C57BL/6 mice. Mice were given chlorpromazine to suspend thermoregulation and lipopolysaccharide to stimulate cytokine production. Core temperature was maintained at 32°C or 37°C for 6 hrs by adjusting environmental temperature. In separate experiments, lipopolysaccharide-treated mice were kept in a cooling chamber without chlorpromazine treatment. Plasma and organs were collected for cytokine quantitation. Chlorpromazine-treated hypothermic mice had 2.3-fold and 1.8-fold higher plasma interleukin-6 and interleukin-10 levels at 6 hrs compared with identically treated normothermic mice (p < .05), whereas plasma tumor necrosis factor-α and interleukin-1β were not significantly different at 2 hrs or 6 hrs. Liver tumor necrosis factor-α and interleukin-6 were significantly higher in hypothermic vs. normothermic mice, but lung and brain cytokines were not different. Lipopolysaccharide-treated mice kept in a cooling chamber without chlorpromazine treatment developed varying degrees of hypothermia with associated increases in plasma interleukin-6 and interleukin-10. A nonspecific marker of stress (plasma corticosterone) was not affected by hypothermia in lipopolysaccharide-treated mice. Further studies are necessary to determine the mechanism and physiologic consequences of augmented systemic interleukin-6 and interleukin-10 expression during induced hypothermia.
