The fetal inflammatory response syndrome plays a central role in the pathogenesis of white matter damage, i. e. cystic periventricular leukomalacia (PVL) in the preterm infant. High levels of proinflammatory cytokines including interleukin-6 (IL-6) have been observed in autopsies of brains of these infants. Thus, an association between IL-6 -174 (G/C) polymorphism, affecting IL-6 transcription rate and plasma cytokine levels, and development of PVL might be hypothesized. We found a significant increased rate of homozygous carriers of the IL-6-174C mutation in mothers with chorioamnionitis and preterm birth with subsequent development of cystic PVL. It could be hypothesized that in pregnant women, who are homozygous carriers of the IL-6-174C mutation, chorioamnionitis could lead to change in the release of the proinflammatory cytokine IL-6. This augmented or secondary up-regulated cytokine could cause a boosted inflammatory response syndrome of the fetus with consecutive damage of the white matter. I hope that this research project might open new horizons and encourage hope for new preventive and therapeutic strategies for the prevention of PVL and cerebral palsy in preterm infants.
