IL36G and bacterial infectious disease: The findings that Il36g expression within the alveolar immune cell compartment was restricted to neutrophils in LPS-challenged mice and that stimulation of mouse AMs, mouse neutrophils, and human neutrophils with LPS in vitro increased IL-36γ production demonstrate that neutrophils can also be an important source of IL-36γ in humans and mice in neutrophilic inflammation associated with bacterial infection.