Anti‐Tn Monoclonal Antibody Ameliorates Hyperoxia‐Induced Kidney Injury by Suppressing Oxidative Stress and Inflammation in Neonatal Mice

The Tn antigen, an N‐acetylgalactosamine structure linked to serine or threonine, has been shown to induce high‐specificity, high‐affinity anti‐Tn antibodies in mice. Maternal immunization with the Tn vaccine increases serum anti‐Tn antibody titers and attenuates hyperoxia‐induced kidney injury in neonatal rats. However, immunizing mothers to treat neonatal kidney disease is clinically impractical. This study is aimed at determining whether anti‐Tn monoclonal antibody treatment ameliorates hyperoxia‐induced kidney injury in neonatal mice. Newborn BALB/c mice were exposed to room air (RA) or normobaric hyperoxia (85% O 2 ) for 1 week. On postnatal days 2, 4, and 6, the mice were injected intraperitoneally with PBS alone or with anti‐Tn monoclonal antibodies at 25 μ g/g body weight in 50 μ L phosphate‐buffered saline (PBS). The mice were divided into four study groups: RA + PBS, RA + anti‐Tn monoclonal antibody, O 2 + PBS, and O 2 + anti‐Tn monoclonal antibody. The kidneys were excised for histology, oxidative stress, cytokine, and Western blot analyses on postnatal day 7. The O 2 + PBS mice exhibited significantly higher kidney injury scores, 8‐hydroxy‐2’‐deoxyguanosine (8‐OHdG) and nuclear factor‐ κ B (NF‐ κ B) expression, and cytokine levels than did the RA + PBS mice or RA + anti‐Tn mice. Anti‐Tn monoclonal antibody treatment reduced kidney injury and cytokine levels to normoxic levels. The attenuation of kidney injury was accompanied by a reduction of oxidative stress and NF‐ κ B expression. Therefore, we propose that anti‐Tn monoclonal antibody treatment ameliorates hyperoxia‐induced kidney injury by suppressing oxidative stress and inflammation in neonatal mice.