Campbell RA, et al. - Given that neutrophil-mediated inflammation can cause inflammatory tissue damage, researchers tested the premises that preterm neonatal PMNs fail to synthesize IL-6Rα due to alterations in mammalian target of rapamycin (mTOR) signaling. Using ELISA, real-time RT-PCR, western blotting, flow cytometry, and immunocytochemistry with phospho-specific antibodies, IL-6Rα expression, PAF receptor expression, and mTOR signaling in plasma and PAF-stimulated PMNs isolated from newborn infants and healthy adults were studied. Findings revealed that neonate plasma contains significantly less soluble IL-6Rα vs healthy adults. According to results, preterm neonatal PMNs show reduced mTOR pathway signaling leading to lowered IL-6Rα synthesis. Findings suggested that decreased synthesis of IL-6Rα by neonatal PMNs might lead to reduced IL-6/IL-6Rα trans-signaling with prolonged inflammatory response and increased morbidity