Thermal stress and prior upper respiratory tract infection are both risk factors for SIDS.

Elevated body temperature and Il-1β and IL-6, the likely mediators of thermal stress and adverse effects of prior infection, both prolong the laryngeal chemoreflex in neonatal decerebrate piglets.

Thermal prolongation of the laryngeal chemoreflex and cytokine-mediated prolongation of the laryngeal chemoreflex interact to amplify the effect of each other and markedly prolong the laryngeal chemoreflex.

Both cytokine-mediated and thermal prolongation are likely to be mediated through TRPV1 receptors expressed presynaptically on C-fiber afferents that, in part, mediate the laryngeal chemoreflex.