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Vagal afferents modulate cytokine-mediated respiratory control at the neonatal medulla oblongata

Kannan V Balan1, Prabha Kc, Zana Hoxha

  • 1Department of Pediatrics, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA.

Respiratory Physiology & Neurobiology
|March 15, 2011
PubMed

Insights

Exposure to endotoxin in immature lungs increases inflammatory cytokines in the brainstem, impairing the ventilatory response to hypoxia in preterm infants. This inflammation affects respiratory control and may contribute to apnea of prematurity.

Area of Science:

  • Neonatal physiology
  • Neuroinflammation
  • Respiratory control

Background:

  • Perinatal sepsis and inflammation cause lung and brain injury in preterm infants.
  • Apnea of prematurity is a significant clinical challenge linked to perinatal insults.

Purpose of the Study:

  • To investigate the effect of endotoxin exposure on proinflammatory cytokine mRNA expression in the medulla oblongata.
  • To determine the association between endotoxin-induced inflammation and impaired respiratory control.

Main Methods:

  • Rat pups were intratracheally exposed to lipopolysaccharide (LPS) or saline.
  • Medulla oblongatas were harvested to quantify cytokine mRNA expression (IL-1β, IL-6).
  • Ventilatory response to hypoxia was assessed using whole-body flow plethysmography.

Main Results:

  • LPS exposure significantly increased medullary mRNA for IL-1β and IL-6.
  • Vagotomy partially blunted the LPS-induced increase in IL-1β mRNA.
  • LPS-exposed pups exhibited an attenuated ventilatory response to hypoxia, even after carotid sinus nerve transection.
  • Increased IL-1β immunochemical expression was observed in the nucleus of the solitary tract and area postrema.

Conclusions:

  • Intratracheal endotoxin exposure upregulates proinflammatory cytokines in the medulla oblongata of rat pups.
  • The upregulation of IL-1β is vagally mediated, while IL-6 is not.
  • Endotoxin exposure is associated with an impaired hypoxic ventilatory response, suggesting a link between neuroinflammation and respiratory dysfunction.

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