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Vancomycin Is Protective in a Neonatal Mouse Model of Staphylococcus epidermidis-Potentiated Hypoxic-Ischemic Brain Injury

Journal article
Authors Jacqueline Lai
Pernilla Svedin
C. Joakim Ek
Amin Mottahedin
Xiaoyang Wang
O. Levy
A. Currie
T. Strunk
Carina Mallard
Published in Antimicrobial Agents and Chemotherapy
Volume 64
Issue 3
Pages 15
ISSN 0066-4804
Publication year 2020
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 15
Language en
Keywords Staphylococcus epidermidis, bacterial infection, sepsis, hypoxia-ischemia, neonatal mice, vancomycin, pentoxifylline, brain, injury, neuroprotection, preterm, cerebral-blood-flow, pentoxifylline treatment, rat model, mice, activation, inflammation, sepsis, aureus, vulnerability, increases, Microbiology, Pharmacology & Pharmacy
Subject categories Pharmacology and Toxicology


Infection is correlated with increased risk of neurodevelopmental sequelae in preterm infants. In modeling neonatal brain injury, Toll-like receptor agonists have often been used to mimic infections and induce inflammation. Using the most common cause of bacteremia in preterm infants, Staphylococcus epidermidis, we present a more clinically relevant neonatal mouse model that addresses the combined effects of bacterial infection together with subsequent hypoxic-ischemic brain insult. Currently, there is no neuroprotective treatment for the preterm population. Hence, we tested the neuroprotective effects of vancomycin with and without adjunct therapy using the anti-inflammatory agent pentoxifylline. We characterized the effects of S. epidermidis infection on the inflammatory response in the periphery and the brain, as well as the physiological changes in the central nervous system that might affect neurodevelopmental outcomes. Intraperitoneal injection of postnatal day 4 mice with a live clinical isolate of S. epidermidis led to bacteremia and induction of proinflammatory cytokines in the blood, as well as transient elevations of neutrophil and monocyte chemotactic cytokines and caspase 3 activity in the brain. When hypoxia-ischemia was induced postinfection, more severe brain damage was observed in infected animals than in saline-injected controls. This infection-induced inflammation and potentiated brain injury was inoculum dose dependent and was alleviated by the antibiotic vancomycin. Pentoxifylline did not provide any additional neuroprotective effect. Thus, we show for the first time that live S. epidermidis potentiates hypoxic-ischemic preterm brain injury and that peripheral inhibition of inflammation with antibiotics, such as vancomycin, reduces the extent of brain injury.

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