Inflammation induced by alarmins released from injured/necrotic cells. A. Injured/necrotic cells with membrane breaks release ATP and mitochondrial alarmins (mitochondrial products). B. Extracellular ATP stimulates in target (immune) cells the assembly of the NALP3 inflammasome via its interaction with the P2X7 receptor, activating caspase-1. Mitochondrial (mt)DNA stimulates the transcription of the pro-IL-1ß gene via its interaction with TLR9 receptor, and the production of pro-IL-1ß that will be cleaved by activated caspase-1 into bioactive IL-1ß, which in turn can be released into the alveolar space and the interstitium and generate local inflammation. fMLP will create chemotactic gradients to attract neutrophils to the injured tissues. C. Neutrophils attracted to the injured tissues will be activated further by fMLP and IL-1ß via their respective receptors (FPR1, and IL-1R), generate oxidative burst and release proteases, which could be further deleterious to tissues (neutrophil-dependent tissue injury).