Adverse childhood experiences (ACEs) confer risk for negative mental and physical health outcomes across the life course. ACEs may confer this risk by affecting the functional connectivity of corticolimbic brain circuits implicated in threat processing, emotion regulation, contextual memory, and peripheral physiological regulation. Critically, the biological pathways that link ACEs to the brain are not well understood. The present study addresses this knowledge gap by considering mediators of systemic inflammation, in particular the proinflammatory cytokine interleukin(IL)-6, which may be increased following ACEs and may also influence corticolimbic brain circuits. In accordance with prior theoretical accounts, it was hypothesized that circulating IL-6 would statistically link retrospective reports of ACEs to corticolimbic connectivity in adulthood. Participants were 303 healthy midlife adults who retrospectively reported ACEs, underwent a blood draw to assess circulating IL-6, and underwent resting-state fMRI. Hierarchical linear regression analyses controlling for age, sex, race, BMI, and participant motion tested whether retrospectively reported ACEs predicts circulating IL-6 and resting corticolimbic connectivity, as well as whether circulating IL-6 predicts resting corticolimbic connectivity. Ancillary analyses tested whether corticolimbic connectivity associated with subclinical depressive symptoms, as well as whether ACEs moderated any brain-inflammation associations. Retrospective reports of physical abuse associated with IL-6 (β(SE) = 0.14(0.05), p = 0.009), but not with corticolimbic connectivity (p = 0.165). IL-6 associated negatively with connectivity in a corticolimbic circuit comprising the amygdala, hippocampus, ventromedial prefrontal cortex, and subgenual anterior cingulate cortex (β(SE) = -0.17(0.06) p = 0.006). Subclinical depressive symptoms were unrelated to corticolimbic connectivity (p > 0.75) and ACEs did not moderate any brain-inflammation associations (p > 0.29). These findings agree with studies linking ACEs to systemic inflammation and systemic inflammation to adult functional connectivity, yet they diverge from those linking ACEs and adult functional connectivity. Collectively, these results do not fully support theoretical accounts linking ACEs to adult corticolimbic connectivity via systemic inflammation.