Myeloid differentiation factor-88−/−(33 (link)), MyD88flox/flox mice (kindly provided by Dr. Matthias Muller and Franco di Padova) were used to generate MyD88 x Acid/AQP5 cre mice, which lack MyD88 in alveolar epithelial type 1 cells (34 (link)) as described (6 (link)), IL-1α- and IL-1β-deficient mice were provided by Dr. Yoichiro Iwakura (35 (link)), IL-18−/− from Jackson laboratory, and C57BL/6 littermate control (WT) mice were used for the study. Mice were housed and bred in pathogen-free animal facility at Transgenose Institute (TAAM-CNRS, UPS 44 under agreement D-45-234-6, 2014), Orleans, France. Mice were bred in a temperature controlled (23°C) facility with strict 12 h light/dark cycles and were given free access to food and water. Female mice (8–10-month-old) were used in this study. Animal experiments were performed with the approval of the French Institutional Ethical Committee under agreement CLE CCO 2015-1088.
To block IL-1α, we used an anti-mouse-IL-1α antibody (Clone ALF-161, eBioscience) and its isotype, armenian hamster IgG (clone eBio299Arm, eBioscience) by intra-peritoneal injection given at 200 μg/mouse, 12 h before ozone exposure.
Recombinant mouse IL-1α (rmIL-1α) (Biolegend 575004, 0.8 μg/mice) was instilled intratracheally (i.t.) 4 h after ozone exposure.
To block IL-1α, we used an anti-mouse-IL-1α antibody (Clone ALF-161, eBioscience) and its isotype, armenian hamster IgG (clone eBio299Arm, eBioscience) by intra-peritoneal injection given at 200 μg/mouse, 12 h before ozone exposure.
Recombinant mouse IL-1α (rmIL-1α) (Biolegend 575004, 0.8 μg/mice) was instilled intratracheally (i.t.) 4 h after ozone exposure.
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