IL1R1 and serum lipopolysaccharide activity: Taken together, our results from different doses of LPS (Fig. 1), plus data from mutant mice (Figs. 2 and 3), strongly indicate a critical role of the NLRP3-IL1β-IL-1R1 pathway in mediating the transition from acute to chronic neuroinflammation incited by severe endotoxemia.