JCI - IL-1R1/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice

IL-1R1/MyD88 signaling and the inflammasome are essential in pulmonary inflammation and fibrosis in mice

Pamela Gasse, Caroline Mary, Isabelle Guenon, Nicolas Noulin, Sabine Charron, Silvia Schnyder-Candrian, Bruno Schnyder, Shizuo Akira, Valérie F.J. Quesniaux, Vincent Lagente, Bernhard Ryffel, Isabelle Couillin

Published in Volume 117, Issue 12

J Clin Invest. 2007; 117(12):3786–3799 doi:10.1172/JCI32285

Abstract | Full text | PDF | Supplemental material

Options: View larger image (or click on image)

Figure 1

Reduced neutrophil and lymphocyte recruitment in the bronchoalveolar space of BLM-challenged MyD88^–/– and IL-1R1^–/– mice.

(A) Total cell counts were augmented at day 1 in BLM-treated WT (B6) mice (15 mg/kg i.n.) and further increased at days 7 and 11 after BLM administration in WT mice, but less so in MyD88^–/– and IL-1R1^–/– mice. (B) Neutrophils were recruited into BALF in WT mice within 24 hours, persisted over 7 days, and normalized on day 11, while only few neutrophils were detected in the absence of MyD88 or IL-1R1. (C) Lymphocytes were found in BALF at day 7 and persisted until day 11 in WT mice and were less prominent in MyD88^–/– and IL-1R1^–/– mice. (D) Alveolar macrophages were augmented at day 11 in WT but not MyD88^–/– or IL-1R1^–/– mice. Data are from 1 experiment representative of 3 independent experiments (n = 4 mice per group; *P < 0.05; **P < 0.01).