Mycobacterium tuberculosis is a major human pathogen responsible for about two million deaths per year. The only available vaccine is the live attenuated strain M. bovis Bacille Calmette Guérin (BCG) that partially protects against pulmonary tuberculosis (TB). Mycobacteria are intracellular pathogens that are able to parasitize macrophages. The inflammatory process induced by mycobacterial infection also recruits neutrophils. Although neutrophils may directly kill some bacilli, this is not the major control they exert on mycobacterial infections. Neutrophils are able to shuttle BCG to the draining lymph node. They crosstalk with dendritic cells to increase BCG antigen presentation and modify cytokine expression profile. Neutrophils help in the early organization of mycobacterial granulomas that are key structures to contain bacilli. However, neutrophils are Janus-like cells that also have detrimental effects on Mycobaterium tuberculosis (Mtb) infection. Neutrophil accumulation in lungs correlates with Mtb high susceptibility in mice and with active pulmonary TB in humans. Mouse neutrophils secrete anti-inflammatory IL-10 upon mycobacterial stimulation that counters Mtb control. Recent discoveries have shown that Myeloid Derived Suppressor Cells - another granulocytic cell population close to neutrophils and exerting strong T cell suppression – are also recruited upon BCG vaccination in the mouse model which opens new perspectives on the key role played by granulocytes on the mycobacterial immune control