First, we quantified IL-1β and IL-18 as the main products of canonical NLRP3 activation and observed that IL-1β showed an increasing pattern as disease progressed in WT animals reaching significantly higher levels in WT than in their NLRP3−/− counterparts only at 8 weeks of infection (2417 ± 752 pg/ml and 953 ± 242 pg/ml, respectively) (Fig. 4a). Here, IL1B is linked to infection.