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 3
Resident radioresistant cells mediate BLM-induced acute inflammation into lung and bronchoalveolar space. Bone marrow chimeras were prepared by lethal irradiation of either WT or MyD88^–/– mice, followed by bone marrow cell reconstitution. WT bone marrow reconstitution of irradiated MyD88^–/– mice (WT→KO) did not restore neutrophil recruitment to the BAL (A) or to the lung parenchyma (B) after BLM administration (15 mg/kg i.n.). Irradiated WT mice reconstituted with MyD88^–/– bone marrow (KO→WT) displayed reduced neutrophil influx in BAL (A) and lung parenchyma (B) compared with WT controls (WT→WT). WT bone marrow reconstitution of irradiated MyD88^–/– mice (WT→KO) did not restore IL-1β (C), KC (D), or IL-6 (E) productions in lung parenchyma. Neutrophil recruitment into the BAL, MPO activity (measured as optical density [OD]), and cytokine and chemokine lung levels were evaluated 24 hours after BLM administration, as described above. Data represent mean values ± SD from 2 independent experiments (n = 4 mice per group; *P < 0.05; **P < 0.01; ns, not significant).