Sepsis is a leading cause of mortality. Plasma cytokine levels may identify those at increased risk of mortality from sepsis. Our aim was to understand how obesity alters cytokine levels during early sepsis and its correlation with survival. Six-week-old C57BL/6 male mice were randomized to control (non-obese) or high fat diet (obese) for 5-7 weeks. Sepsis was induced by cecal ligation and perforation (CLP). Cytokine levels were measured from cheek bleeds 8 h after CLP, and mice were monitored for survival. Other cohorts were sacrificed 1 h after CLP for plasma and tissue. Septic obese mice had higher survival. At 8 h after sepsis, obese mice had higher adiponectin, leptin, and resistin but lower TNFα and IL-6 compared to non-obese mice. When stratified by 24-h survival, adipokines were not significantly different in obese and non-obese mice. TNFα and IL-6 were higher in non-obese, compared to obese, mice that died within 24 h of sepsis. Diet and to sepsis significantly impacted the cecal microbiome. IL-6 is a prognostic biomarker during early sepsis in non-obese and obese mice. A plausible mechanism for the survival difference in non-obese and obese mice may be the difference in gut microbiome and its evolution during sepsis.

中文翻译：

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肥胖改变脓毒症小鼠的细胞因子信号传导和肠道微生物组。

败血症是死亡的主要原因。血浆细胞因子水平可以识别那些因败血症死亡风险增加的人。我们的目的是了解肥胖如何改变早期脓毒症期间的细胞因子水平及其与生存的相关性。六周大的 C57BL/6 雄性小鼠被随机分为对照（非肥胖）或高脂肪饮食（肥胖），为期 5-7 周。盲肠结扎穿孔（CLP）诱发脓毒症。CLP 后 8 小时从脸颊出血中测量细胞因子水平，并监测小鼠的存活情况。其他队列在 CLP 后 1 小时处死以获取血浆和组织。脓毒症肥胖小鼠的存活率较高。脓毒症后 8 小时，与非肥胖小鼠相比，肥胖小鼠的脂联素、瘦素和抵抗素较高，但 TNFα 和 IL-6 较低。当按 24 小时存活率分层时，脂肪因子在肥胖和非肥胖小鼠中没有显着差异。与脓毒症 24 小时内死亡的肥胖小鼠相比，非肥胖小鼠的 TNFα 和 IL-6 更高。饮食和败血症显着影响盲肠微生物组。IL-6 是非肥胖和肥胖小鼠早期败血症期间的预后生物标志物。非肥胖和肥胖小鼠生存差异的一个可能机制可能是肠道微生物组及其在脓毒症期间进化的差异。