IL1B and acute respiratory distress syndrome: Introducing bacterial membrane vesicles (prokaryotic EV analogs) into the nasal cavities of healthy mice stimulates lung inflammation by increasing inflammatory cytokines (e.g., IL-8, IL-6, ICAM-1, pro-IL-1β, and TNF-α) and neutrophil levels, in a process where cytokines positively increase neutrophil lung infiltration and both cytokines and neutrophil levels act to promote ALI/ARDS progression [99].