Interleukin-1beta depresses hypoxic gasping and autoresuscitation in neonatal DBA/1lacJ mice.

The pro-inflammatory cytokine interleukin-1beta (IL-1beta) has been proposed to act as an important mediator between infection and apnea in neonates. In this study, respiration and the ability to survive anoxic challenge were investigated between 70 and 95 min after intraperitoneal injection of IL-1beta (10 microg/kg) or NaCl in 9-day-old DBA/1lacJ mice. Using flow plethysmography, we show that mice given IL-1beta exhibited a decreased tidal volume (V(T)) and minute ventilation (V(E)) during normoxia compared to control animals. Hyperoxic challenge revealed functioning peripheral chemoreceptors in all animals, suggesting a central mechanism underlying the ventilatory effects of IL-1beta. In response to anoxia (100% N2), all animals irrespective of treatment displayed a biphasic ventilatory pattern. Mice given IL-1beta exhibited fewer gasps and were unable to sustain gasping efforts for as long as control animals. Additionally, they were less able to autoresuscitate and survive following severe hypoxic apnea. These findings indicate that infection may adversely affect central respiratory control in newborn mice via interleukin-1beta.