Recent studies suggest that stress can lead to variations in offspring development. However, whether paternal systemic inflammation induces phenotypic changes in the offspring remains unclear. Here, we established an in vivo mouse model of systemic inflammation and investigated the long-term consequences on the offspring. Male, but not female offspring derived from inflammatory fathers (LPS-F1) grew faster than those derived from the control fathers (CON–F1). Moreover, the LPS-F1 males had higher capacity for liver regeneration after injury, as indicated by decreased hepatic fibrosis, apoptosis, and increased hepatocyte proliferation upon carbon tetrachloride challenge. Insulin-like growth factor 2 (Igf2), a key mitogen that drives growth and liver regeneration, was significantly upregulated in the livers of male, but not female offspring from fathers with inflammation. Taken together, paternal inflammation alters the hepatic Igf2 expression and reprograms growth and liver regeneration in male but not female offspring.

最近的研究表明，压力可以导致后代发育的变异。但是，尚不清楚父亲的全身性炎症是否在后代中引起表型改变。在这里，我们建立了一个体内小鼠的全身炎症模型，并研究了对后代的长期后果。源自发炎父亲（LPS-F1）的雄性而非雌性后代的生长速度快于来自对照父亲（CON-F1）的雄性。此外，LPS-F1雄性小鼠在受伤后具有更高的肝再生能力，这表现为四氯化碳激发后肝纤维化，凋亡减少和肝细胞增殖增加。胰岛素样生长因子2（Igf2）是驱动生长和肝脏再生的关键促分裂原，在雄性肝脏中明显上调，而在患有炎症的父亲的雌性后代中则没有。综上所述，父本炎症会改变雄性但非雌性后代的肝Igf2表达并重编程生长和肝脏再生。