Immunization with anti-Tn immunogen in maternal rats protects against hyperoxia-induced kidney injury in newborn offspring.

Abstract

Neonatal hyperoxia increases oxidative stress and adversely disturbs glomerular and tubular maturity. Maternal Tn immunization induces anti-Tn antibody titer and attenuates hyperoxia-induced lung injury in neonatal rats. We intraperitoneally immunized female Sprague-Dawley rats (6 weeks old) with Tn immunogen (50 μg/dose) or carrier protein five times at biweekly intervals on 8, 6, 4, 2, and 0 weeks before the delivery day. The pups were reared for 2 weeks in either room air (RA) or in 85% oxygen-enriched atmosphere (O2), thus generating four study groups, namely carrier protein + RA, Tn vaccine + RA, carrier protein + O2, and Tn vaccine + O2. On postnatal day 14, the kidneys were harvested for the oxidative stress marker 8-hydroxy-2'-deoxyguanosine (8-OHdG), nuclear factor-κB (NF-κB), and collagen expression and histological analyses. Hyperoxia reduced body weight, induced tubular and glomerular injuries, and increased 8-OHdG and NF-κB expression and collagen deposition in the kidneys. By contrast, maternal Tn immunization reduced kidney injury and collagen deposition in neonatal rats. Furthermore, kidney injury attenuation was accompanied by a reduction in 8-OHdG and NF-κB expression. Maternal Tn immunization protects against hyperoxia-induced kidney injury in neonatal rats by attenuating oxidative stress and NF-κB activity. Hyperoxia increased nuclear factor-κB (NF-κB) activity and collagen deposition in neonatal rat kidney. Maternal Tn immunization reduced kidney injury as well as collagen deposition in neonatal rats. Maternal Tn immunization reduced kidney injury and was associated with a reduction in 8-hydroxy-2'-deoxyguanosine and NF-κB activity. Tn vaccine can be a promising treatment modality against hyperoxia-induced kidney injury in neonates.