Alternatively, our lab observed that NLRP3 inflammasome priming in lung neutrophils during S. pneumoniae-induced pneumonia was dominated by host-derived TNF-α secreted by alveolar macrophages (Figure 2A) [94], although TNF-α has been shown to exhibit weaker and delayed ability to prime NLRP3 inflammasome in macrophages as compared with LPS [103]. This evidence concerns the gene TNF and pneumonia.