Developmental differences in the role of interleukins in hyperoxic lung injury in animal models.

Interleukins (IL) are part of the group of immune mediators known as cytokines. IL are produced by many different cells and possess a wide spectrum of biological activities. This review will be focused on the role of IL-1 to 6, 8, 10-13 as it pertains to the effects of hyperoxia on the adult and newborn lung in animal models. Hyperoxic exposure to the adult and newborn lung had variable effects on the expression of IL-1alpha and IL-1beta. Increased IL-6 levels were seen in adult lungs by day 3 and in the newborn lungs by day 10 of exposure to hyperoxia. IL-8 also peaked around day 10 in the newborn lung but there were no significant changes in IL-10. Pretreatment with IL-1, endotoxin, rhSOD, lidocaine, lisofylline, pentoxifylline and overexpression of IL-6, 11, and 13 seemed to attenuate hyperoxic lung injury in the adult. This protection was accompanied by increased pulmonary MnSOD, VEGF expression and decreased apoptosis. It is clear that IL have a significant role to play in hyperoxic lung injury. Increased IL expression and release has a cascade effect and appears to predate the influx of inflammatory cells. There are significant differences in the type and timing of IL expression and release in the adult and newborn lung in response to hyperoxia. Designing a therapeutic approach to counteract oxygen toxicity in the immature lung first needs understanding of the unique responses in the newborn.