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Sleep has a strong impact on both humoral and cellular immunity, but its acute effects on innate immune defense remain unclear. Here we elucidated in mice whether sleep affects innate immune cells and defense against systemic infection. Mice were allowed to sleep for 6 h at the beginning of the resting phase and compared to mice being awake for the same time. Sleep significantly increased the frequency and absolute cell counts of classical and non-classical monocytes in blood and secondary lymphatic organs whereas neutrophils (PMNs) were unaffected. Changes in monocyte numbers upon sleep compared to wakefulness remained for up to 24 h, did not involve CCR2 signaling and were not caused by impaired myelopoesis or bone marrow egress, cell death, differentiation into macrophages, or redistribution to peripheral tissues. On the contrary, SD also reduced macrophage numbers in spleen, as well as monocyte content in lung and gut. These findings suggest that sleep reduced monocyte adhesion in the marginal pool and promoted monocyte extravasation to peripheral tissues. In a mouse model of systemic bacterial infection to mimic sepsis, the bacterial load in the spleen of sleep mice was significantly reduced throughout the infection. Consequently, sleep significantly increased survival upon infection. These data provide evidence that sleep maintains homeostasis and function of innate immune cells thereby supporting early defense against bacterial pathogens. [ABSTRACT FROM AUTHOR]