IL-1R1/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice
J. Clin. Invest. Pamela Gasse, et al. 117:3786 doi:10.1172/JCI32285 [Go to this article.]

Figure 2
Reduced BLM-induced acute lung inflammation in IL-1R1– and MyD88-deficient mice. IL-1R1– and MyD88-deficient mice showed reduced neutrophil recruitment in BALF (A) and lung tissue (B), whereas IL-18R–deficient mice had neutrophil counts comparable to WT mice (C). BALs were performed 24 hours after BLM instillation (15 mg/kg), and MPO activity was analyzed at day 7. IL-1β (D), KC (E), and IL-6 (F) in the lung at 24 hours were reduced in IL-1R1– and MyD88-deficient mice as compared with WT mice. Cytokine and chemokine quantification in lung homogenates were performed by multiplex ELISA cytokine arrays (detection limit at 1 pg/ml). Data represent mean values ± SD from 2 independent experiments (n = 4 mice per group; *P < 0.05; **P < 0.01).