It is well established that protective neutrophil effector functions during infection can be accompanied by severe collateral damage due to their tissue damaging properties by releasing inflammatory mediators such as IL-1β (Liu and Sun, 2019) and reactive oxygen species (Kolaczkowska and Kubes, 2013) or via tissue-factor mediated activation of coagulation (Maugeri and Manfredi, 2015; Østerud, 2010; Pawlinski and Mackman, 2010) and the release of neutrophil extracellular traps (NETs) (Kimball et al., 2016; Yipp and Kubes, 2013). Here, IL1B is linked to infection.