The COVID-19 pandemic has highlighted the role of breastfeeding in providing passive immunity to infants via specific anti-SARS-CoV-2 antibodies in breast milk. We aimed to quantify these antibodies across different lactation stages and identify influencing factors. This prospective study involved mother–child dyads from Innsbruck University Hospital, Austria, with a positive maternal SARS-CoV-2 test during pregnancy or peripartum between 2020 and 2023. We collected breast milk samples at various lactation stages and analyzed anti-Spike S1 receptor-binding domain (S1RBD) immunoglobulins (Ig). Maternal and neonatal data were obtained from interviews and medical records. This study included 140 mothers and 144 neonates. Anti-S1RBD-IgA (72.0%), -IgG (86.0%), and -IgM (41.7%) were highly present in colostrum and decreased as milk matured. Mothers with natural infection and vaccination exhibited higher anti-S1RBD-IgA and -IgG titers in all milk stages. Mothers with moderate to severe infections had higher concentrations of anti-S1RBD-IgA and -IgG in transitional milk and higher anti-S1RBD-IgA and -IgM in mature milk compared to those with mild or asymptomatic infections. Variations in antibody responses were also observed with preterm birth and across different virus waves. This study demonstrates the dynamic nature of breast milk Ig and underscores the importance of breastfeeding during a pandemic.

Neonatal brain injury remains a significant issue with limited treatment options. This study investigates the potential of the endogenous neurosteroid dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) as neuroprotective agents, building on evidence of their mechanisms in adult brain injury models. The primary objective was to evaluate their neuroprotective and anti-oxidative properties in a mouse model of neonatal hypoxic–ischemic brain injury. Using the modified Rice–Vannucci model, brain injury was induced in 7-day-old mouse pups, followed by treatment with various concentrations of DHEA and DHEAS (0.1, 1, and 10 µg/g body weight) via intraperitoneal injection after a 2 h recovery period. Mice were sacrificed after 24 hours for analysis of somatometry, brain injury, apoptosis, microglial activation, and oxidative stress markers (NOX2, 4-HNE, 8-OHdG), along with the anti-oxidant marker SOD1. While no statistically significant effects of DHEA or DHEAS were observed at the tested doses and time points, the absence of toxic or adverse effects highlights their safety profile. These findings provide a foundation for further research into optimizing dosing strategies, timing, and delivery methods. Future studies should refine these variables to maximize neuroprotective efficacy, investigate DHEA(S)’ exact mechanisms of action, and explore their potential for clinical application in neonatal care.

Neonatal brain injury remains a significant issue with limited treatment options. The endogenous neurosteroids dehydroxyepiandrosterone (DHEA) and its sulfate ester (DHEAS) have demonstrated promising therapeutic potential in adult brain injury models due to their neuroprotective mechanisms. This study aimed to analyze the neuroprotective potential of DHEA and DHEAS with a particular interest in anti-oxidative properties in a mouse model of neonatal hypoxic-ischemic brain injury. Using the modified Rice-Vanucci model, brain injury was induced in 7-day-old mouse pups, followed by treatment with various concentrations of DHEA and DHEAS (0.1, 1, and 10 µg/g body weight) via intraperitoneal injection after a 2-hour recovery period. Mice were sacrificed after 24 hours for analysis of somatometry, brain injury, apoptosis, microglial activation, and oxidative stress markers (NOX2, 4-HNE, 8-OHdG), along with the anti-oxidant marker SOD1. No statistically significant effects of the treatments were observed at the tested doses and time points. Although this study did not conclusively demonstrate the anti-oxidative neuroprotective potential of DHEA or DHEAS, neither substance exhibited toxic or harmful effects. Several factors may have contributed to the lack of observable effects, underscoring the need for further refinement in future studies of DHEA(S) and other treatments of neonatal hypoxic-ischemic brain injury.