Maternal Low- and High-Fat Diets Reduce Neonatal Mouse Survival in S. epidermidis Sepsis, Altering Cytokine Signaling

Neonatal sepsis remains a leading cause of morbidity and mortality in infants, particularly in premature or immunocompromised newborns. Staphylococcus epidermidis is a common pathogen in neonatal intensive care units, often causing bloodstream infections. Maternal malnutrition, encompassing both undernutrition and overnutrition, is known to increase offspring susceptibility to infections and mortality, but the underlying mechanisms are not fully understood. This study investigates how maternal dietary fat content impacts the immune response and survival of neonatal mice challenged with S. epidermidis sepsis, focusing on cytokine signaling and metabolomic pathways as potential mediators of vulnerability.

Researchers evaluated bacterial burden and serum cytokine levels in septic neonatal mice born to dams fed diets with different dietary fat content. 6-week-old dams were fed either a low-fat diet (LFD) or a high-fat diet (HFD), presumably compared to a control diet (though not explicitly stated as 'normal' in the abstract). Following birth, offspring were subjected to Staphylococcus epidermidis sepsis. Primary endpoints included neonatal survival rates, basal serum cytokine levels, and changes in cytokine elevation during sepsis. Additionally, metabolomic pathway analysis was performed on offspring to identify altered metabolic processes.

Maternal dietary fat content significantly impacted neonatal outcomes during sepsis. Both maternal LFD and HFD led to decreased survival rates in neonatal mice challenged with Staphylococcus epidermidis sepsis. The study observed changes in basal serum cytokine levels in offspring from both diet groups, indicating altered immune homeostasis even before infection. Specifically, maternal HFD caused decreased cytokine elevation during sepsis, suggesting a blunted or dysregulated inflammatory response crucial for pathogen clearance. Furthermore, maternal LFD and HFD were found to alter similar metabolomic pathways in offspring, implying common metabolic vulnerabilities despite differing dietary fat compositions. These metabolic shifts likely contribute to the observed immune dysfunction and increased susceptibility to sepsis. While specific numerical data for survival percentages, cytokine fold-changes, or p-values are not provided in the abstract, the qualitative findings are clear.

Maternal low-fat and high-fat diets both decreased survival during neonatal sepsis and altered serum cytokine responses, with HFD specifically blunting cytokine elevation.