LAUSR

Experiencing maltreatment, abuse and/or neglect during childhood (CM) is associated with adverse health outcomes later in life. A state of chronic low-grade inflammation and alterations in inflammatory processes were suggested to be involved in the high prevalence of secondary diseases observed with CM. The molecular mechanisms underlying the establishment of this pro-inflammatory phenotype remain, however, largely unknown. On a cellular level, mitochondria were recently found to be not only the main energy suppliers of human cells, but also key regulators of inflammatory processes. We therefore analyzed in a study cohort of 30 women with varying degrees of CM experiences, whether mitochondrial activity was altered in immune cells and was associated with increased levels of inflammation. With increasingly severe CM experiences, study participants displayed higher levels of endogenous, bioactive molecules linked to oxidative stress and an increased immune cell mitochondrial activity, which was associated with a higher secretion of the pro-inflammatory cytokines IL-1beta, IL-6, and TNF-alpha. Together these data support the hypothesis that alterations in immune cell mitochondrial functioning might be at the interface between the association of CM experiences and a state of chronic low-grade inflammation that persists until adulthood. The present findings further emphasize that the early prevention of child maltreatment, abuse and neglect warrants more attention, as affected individuals suffer not only from life-long consequences for mental, but also for physical health.