Lack of aromatase improves cell-mediated immune response after burn

Persistent elevation of estrogens after injury or sepsis correlates with increased mortality and a pro-inflammatory state. Given that aromatase is elevated after injury, the enzyme's subsequent conversion of androstenedione and testosterone to estrone and estradiol may be a causative factor for this correlation.

Aromatase knockout (ArKO) and wild type female mice were subjected to a 15% total body surface area burn. The delayed type hypersensitivity (DTH) response and splenocyte production of IL-6 and TNFalpha were examined 8 days later.

Injury in wild type mice is associated with an impairment in the DTH response, as well as with an increase in IL-6 and TNFalpha production by stimulated splenocytes. However, for ArKO mice, the impairment in DTH was blunted and there was no difference in IL-6 production between sham- and burn-injured mice. Sham-injured ArKO mice produced nearly 50% more TNFalpha than wild type mice, while injury did not result in a significant increase in TNFalpha production for ArKO mice.

The complete deficiency in aromatase correlated with a decrease in the production of the inflammatory cytokine IL-6 and partial restoration of the DTH response after severe burn. However, a deficiency of aromatase did not effect TNFalpha production after injury.