Vagal nerve stimulation attenuates IL-6 and TNFα expression in respiratory regions of the developing rat brainstem

Research output: Contribution to journalArticlepeer-review

Abstract

Pre-term infants are at greater risk for systemic infection due to an underdeveloped immune system. Airway infection results in immune up-regulation of early pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNFα) in the brainstem. Current treatment for neonatal infection involves antibiotic administration. We previously showed that LPS injected into the trachea of neonatal rats causes changes in breathing and in IL-1β expression in the nucleus tractus solitarii (NTS) and hypoglossal motor nucleus (XII). We hypothesize that lipopolysaccharide (LPS) instilled in the trachea also causes the up-regulation of IL-6 and TNFα in the brainstem autonomic control regions. To test this hypothesis we injected LPS into the trachea of rat pups (postnatal ages 10-12 days) and then assessed changes in IL-6 and TNFα. Vagal nerve stimulation has been used in the treatment of many inflammatory disorders, including sepsis. Our experiments show that VNS attenuates the upregulation of IL-6 and TNFα caused by LPS and may be a viable alternative to antibiotics.

Original languageEnglish
Pages (from-to)1-4
Number of pages4
JournalRespiratory Physiology and Neurobiology
Volume229
DOIs
StatePublished - Jul 15 2016

ASJC Scopus Subject Areas

  • General Neuroscience
  • Physiology
  • Pulmonary and Respiratory Medicine

Keywords

  • Inflammation
  • Respiratory control
  • Vagus nerve
  • Animals, Newborn
  • Immunohistochemistry
  • Up-Regulation
  • Inflammation/metabolism
  • Brain Stem/growth & development
  • Rats, Sprague-Dawley
  • Lipopolysaccharides
  • Vagus Nerve Stimulation
  • Animals
  • Tumor Necrosis Factor-alpha/metabolism
  • Interleukin-6/metabolism
  • Respiratory Tract Infections/metabolism
  • Trachea/immunology
  • Disease Models, Animal

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