Blood monocytes are present throughout the body. These cells mediate host antimicrobial defenses and are implicated in almost every inflammatory process. It is accepted that monocytes are non-proliferating myeloid cells and their abundance in peripheral tissues depends on the recruitment from the circulation. However, there is emerging evidence that macrophages can be rescued from cell cycle arrest and actively proliferate during infections to increase population density. These findings may contribute to a novel concept that monocytes are not terminally differentiated cells without the capacity to locally proliferate. However, the proliferation of blood monocytes has not been studied so far and the contribution of recruitment versus local proliferation for the presence of Ly6C+ monocytes in inflamed tissues also needs to be defined.. Furthermore, the function of proliferative monocytes during infection and inflammation is unknown. IL-6 is a pleiotropic cytokine that is known to regulate inflammatory processes and play an essential role during bacterial infections. Role of IL-6 in regulation of monocyte accumulation during bacterial infections is also unknown. This thesis demonstrates the proliferative capacity of recruited Ly6C+ monocytes in a murine model of urinary tract infection and in LPS-induced peritonitis. IL-6 trans-signaling was identified as the key pathway that regulates the proliferation of Ly6C+ monocytes in both inflammatory models. Non-proliferating monocytes phagocytized matured neutrophils, whereas proliferating monocytes critically contribute to the defense against infection. These data reveal the process of monocyte proliferation during bacteria infected tissues and identify IL-6 as the key molecule that regulates this proliferation.