When awake, we perceive stimuli from the external world. When asleep, our brain disconnects from the sensory environment. In contrast to these exteroceptive stimuli, little is known about how interoceptive stimuli are processed by the sleeping brain. The vagus nerve is a mixed sensory-motor nerve that interfaces between the autonomic periphery and the brain. We asked whether stimulating specifically vagal sensory afferents modulates sleep. All experiments are based on viral transfection of vGluT2-expressing neurons in the jugular-nodose ganglion of the left vagus nerve, in combination with polysomnographic, fiber photometry and brain temperature recordings in freely moving conditions. Whole-cell patch-clamp recordings confirmed that optogenetic activation of vagal afferents formed functional glutamatergic synaptic contacts in the nucleus tractus solitarius. We found that chemogenetic activation of the vagal sensory afferents (1.5 or 2.5mg/kg CNO) at ZT0 suppressed rapid-eye-movement sleep (REMS) in a dose-dependent manner, as evident by the lack of its characteristic EEG/EMG correlates. The spectral properties of non-REMS-EEG were affected in a moderate manner. To characterize the physiological correlates of sleep during elevated vagal activity, we measured the cortical brain temperature and found a drop in temperature after vagal sensory stimulation positively correlated with the increase in REMS onset latency. The mechanisms underlying these alterations are addressed using fiber photometry techniques. Our findings point to a major role for vagal afferent activity in body-brain physiology that regulates the balanced expression of non-REMS and REMS. Moreover, they indicate that vagus nerve stimulation could offer non-invasive strategies to improve sleep architecture in pathological conditions.