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Intrapulmonary lipopolysaccharide exposure upregulates cytokine expression in the neonatal brainstem

Authors

  • Kannan V Balan,

    1. Rainbow Babies & Children’s Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH, USA
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  • Prabha Kc,

    1. Rainbow Babies & Children’s Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH, USA
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  • Catherine A Mayer,

    1. Rainbow Babies & Children’s Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH, USA
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  • Christopher G Wilson,

    1. Rainbow Babies & Children’s Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH, USA
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  • Abdelmadjid Belkadi,

    1. Rainbow Babies & Children’s Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH, USA
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  • Richard J Martin

    1. Rainbow Babies & Children’s Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH, USA
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RJ Martin, M.D., Rainbow Babies & Children’s Hospital, 11100 Euclid Avenue, Cleveland, OH 44106-6010, USA.
Tel: 216 844 3387 |
Fax: 216 844 3380 |
Email: rxm6@case.edu

Abstract

Perinatal inflammation and neonatal sepsis trigger lung and brain injury. We hypothesized that endotoxin exposure in the immature lung upregulates proinflammatory cytokine expression in the brainstem and impairs respiratory control. Lipopolysaccharide (LPS) or saline was administered intratracheally to vagal intact or denervated rat pups. LPS increased brainstem IL-1β and vagotomy blunted this response. There was an attenuated ventilatory response to hypoxia and increased brainstem IL-1β expression after LPS.

Conclusion:  Intratracheal endotoxin exposure in rat pups is associated with upregulation of IL-1β in the brainstem that is vagally mediated and associated with an impaired hypoxic ventilatory response.

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