Abstract
Granulocytes are innate immune effector cells with essential functions in host resistance to bacterial infections. I will discuss emerging evidence that during Mycobacterium tuberculosis infection, counter-intuitively, eosinophils are host-protective while neutrophils are host detrimental. Additionally, I will propose a 'tipping-point' model in which neutrophils are an integral part of a feedforward loop driving tuberculosis disease exacerbation.