IL1B and inflammation: The postulated underlying mechanism of GOS leading to inhibition of NLRP3 inflammasome is summarized in Fig. 7I. GOS supplementation can inhibit the activation of NLRP3 inflammasome possibly by downregulating the “TLR4/NF-κB and secondarily MAPK” signaling pathway and reducing the production of ATP and mitochondrial ROS, thereby suppressing caspase-1 activation and preventing lung inflammation (e.g., mature IL-1β release).