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. 2019 Apr 9;15(4):e1007689. doi: 10.1371/journal.ppat.1007689

Fig 5. NLRP3 inflammasome activation plays a crucial role in the pathogenesis of HMPV via IL-1β release.

Fig 5

(A) BALB/c mice were inoculated with HMPV at a lethal dose (106 PFU per mouse) in the presence or absence of MCC950 (5 mg/kg). Immediately after infection, they were injected or not with IL-18BP (75 μg/kg). MCC950 and IL-18BP treatments were repeated for the next two days (1 time/day). The animals were monitored for survival and weight loss for 14 days after infection and euthanized if humane end points were reached (≤ 20% of initial weight). Values are shown as mean of weight ± S.E.M or average percent survival (Kaplan Meier survial curves, *** P < 0.001 MCC950 vs DMSO, n = 10 per group). (B) IL-1β-/- and C57BL/6 (IL-1β+/+) mice were inoculated with HMPV at a LD50 dose (2 x 106 PFU per mouse) in the presence or absence of MCC950 (5 mg/kg). MCC950 treatment was repeated for the next two days (1 time/day). The animals were monitored for survival and weight loss for 14 days after infection and euthanized if humane end points were reached (≤ 20% of initial weight). Values are shown as mean of weight ± S.E.M or average percent survival (Kaplan Meier survial curves, * P < 0.05 IL-1β-/- or IL-1β+/+/MCC950 vs IL-1β+/+, n = 20 per group). (C-E) IFN-γ, total protein and leukocyte recruitment were evaluated in BAL of IL-1β-/- and C57BL/6 (IL-1β+/+) mice. Values are shown as mean ± S.E.M (ANOVA followed by Tukey post hoc, * P < 0.05; ** P < 0.01 IL-1β-/- or IL-1β+/+/MCC950 vs IL-1β+/+, n = 10 per group).