Biology subjects

Bermick, J. R.

Publications and source records attributed to Bermick, J. R..

2 recordsLinked to original sources

bioRxiv2025

Maternal low-fat and high-fat diet decreases survival and alters cytokine signaling in neonatal mice with Staphylococcus epidermidis sepsis

ObjectiveMaternal malnutrition increases susceptibility to sepsis and mortality in neonates. The reason for this increased susceptibility remains unknown. We aimed to evaluate bacterial burden and serum cytokine levels in septic neonatal mice born to dams with malnutrition. Methods6-week-old C57BL/6 dams were placed on a low-fat (LFD) (10% kcal from fat), control (CD) (18% kcal from fat), or high-fat (HFD) (60% kcal from fat) diet for 3 weeks prior to breeding. Sepsis was induced in P4-P6 offspring via intraperitoneal Staphylococcus epidermidis injection. Mice were monitored for survival. At 12h after sepsis, serum and peritoneal wash fluid were collected for bacterial count and serum cytokine levels. In the absence of infection, P4-P6 offspring had untargeted serum metabolomics performed. ResultsSeptic offspring of dams fed LFD and HFD had significantly higher mortality than offspring of dams fed CD. There was no difference in serum or peritoneal wash bacterial loads. Maternal diet and Staphylococcus epidermidis sepsis caused changes in basal serum cytokine levels, with HFD causing decreased cytokine elevation during sepsis. Maternal LFD and HFD altered similar metabolomic pathways in offspring. ConclusionMaternal LFD and HFD decrease survival during neonatal sepsis and alter serum cytokines and the metabolome, supporting a role for maternal nutrition in neonatal immune function and infection susceptibility.

immunology↗

bioRxiv2024

A predominately pulmonary activation of complement in a mouse model of severe COVID-19

Evidence from in vitro studies and observational human disease data suggest the complement system plays a significant role in SARS-CoV-2 pathogenesis, although how complement dysregulation develops in patients with severe COVID-19 is unknown. Here, using a mouse-adapted SARS-CoV-2 virus (SARS2-N501YMA30) and a mouse model of severe COVID-19, we identify significant serologic and pulmonary complement activation following infection. We observed C3 activation in airway and alveolar epithelia, and in pulmonary vascular endothelia. Our evidence suggests that while the alternative pathway is the primary route of complement activation, components of both the alternative and classical pathways are produced locally by respiratory epithelial cells following infection, and increased in primary cultures of human airway epithelia in response to cytokine exposure. This locally generated complement response appears to precede and subsequently drive lung injury and inflammation. Results from this mouse model recapitulate findings in humans, which suggest sex-specific variance in complement activation, with predilection for increased C3 activity in males, a finding that may correlate with more severe disease. Our findings indicate that complement activation is a defining feature of severe COVID-19 in mice and lay the foundation for further investigation into the role of complement in COVID-19.

immunology↗