Mycobacterium tuberculosis (Mtb) is the primary cause of tuberculosis (TB), which is one of the leading causes of infectious disease mortality worldwide [1]. Unlike many bacterial pathogens, Mtb is very slow growing and establishes a chronic infection, often in the lungs. Many immune cell types accumulate at sites of Mtb infection. Granulocytes are abundant innate effector cells that can rapidly enter infected tissues, secrete inflammatory cytokines and lipid mediators, phagocytose pathogens, and excrete extracellular traps. Neutrophils, in particular, are fundamental mediators of host resistance to many bacterial infections. However, recent studies have revealed complex and divergent roles for different granulocyte subsets during Mtb infection. This article will highlight recent advances in our understanding that neutrophils are detrimental during Mtb infection and that eosinophils, typically associated with parasitic infections, are host-protective during TB. Finally, I will propose a ‘tipping-point’ model in which neutrophils are central effector cells in a feed-forward loop of TB disease exacerbation.