It has been suggested that certain metabolic conditions in macrophages could be key to permit intracellular infection. As intracellular bacteria are able to take up nutrients directly from the cytoplasm of infected cells and macrophages should regulate their metabolism to limit bacterial replication, this metabolic tug-of-war between infecting pathogens and their host-cells might determine the final outcome of the infection process. However, these observations were never carried- out at the single-cell level in time-lapse experiments, therefore it was difficult to ascertain in these studies whether macrophages showing a certain metabolic phenotype then permitted or restricted intracellular replication. Our research question therefore is: which are those cellular parameters determining permissiveness or restriction to bacterial infection in human macrophages? To answer this question, we propose to develop an innovative pipeline from wet-lab to in silico analyses, which should allow identifying these parameters.