Specifically, Nod-like receptor-stimulating bacteria present in the GI tract were shown to increase levels of interleukin-17A, which lead to the production of granulocyte–macrophage colony-stimulating factor and killing of bacterial pathogen by alveolar macrophages.19 Enhanced susceptibility to K. pneumoniae in germ-free mice was also associated increased levels of IL-10, decreased neutrophil pulmonary recruitment, and bacterial growth and dissemination.18 However, the rigor of prior research linking alcohol dysbiosis to bacterial pneumonia is limited. Here, IL17A is linked to bacterial pneumonia.