Following the rapid induction and secretion of cytokines and chemokines, including interleukin 1b (IL-1b), traumatic brain injury (TBI) also increases the astrocytic expression of aromatase (estrogen synthase), in birds and mammals.  The neural synthesis of estradiol (E₂) via glial aromatase following TBI is neuroprotective as central inhibition of aromatase increases, and concomitant administration of E₂ reduces; infarct size, lesion volume, and neuronal loss. Surprisingly, the mechanism underlying injury-induced up-regulation and maintenance of astrocytic aromatase remains completely unknown.  Since TBI increases cytokines prior to glial aromatase, we hypothesize that the secretion of cytokines up-regulates astrocytic aromatase in the injured brain. In order to determine if IL-1 signaling is necessary for this induction, we tested the influence of a chronic penetrating injury on the expression of aromatase in both wild type (WT) mice and knockout mice deficient in IL-1 receptors (IL1R-KO). Adult male wild type or IL1R-KO mice were implanted with an unilateral in-dwelling cannula targeted at the hippocampus or were subjected to a sham operation and sacrificed 10 days post-surgery.  Brains were microdissected and total RNA extracted from injured cortex (containing the needle tract), contralateral uninjured cortex, and the cerebellum in implanted and sham animals. Aromatase expression was measured using RT-PCR using GAPDH as control.  Aromatase mRNA was significantly higher in injured cortical samples compared to sham cortical samples for both WT and IL1R-KO mice (p<0.001).  Additionally, aromatase was significantly higher in the injured cortex than the uninjured cerebellum of the same animal (p<0.001), independent of genotype. Interestingly, aromatase was also up-regulated in the contralateral, uninjured cerebrum in animals with cortical injuries, suggesting the injury-induced up-regulation of aromatase may spread beyond the site of the injury. While TBI may have far-reaching effects on aromatase expression, these data suggest that IL-1 signaling is not necessary for the induction of aromatase.