PMC

HA increased AHR in WT mice, but not in (A) TLR4−/−mice, (B) MyD88−/−mice, or (C) TIRAP−/− mice (*p<0.05 vs. vehicle-WT; #p<0.05 vs. HA-WT, N = 5 per group).

HA levels were significantly increased in all ozone-exposed groups (*p<0.01, vs. FA exposed group; #p<0.05, vs. O3-exposed WT, group, N = 4–5 per group).

(A) There were no observed differences in cellular inflammation in the airspace 2 hours after direct challenge to HA, (B) When compared to ozone challenge, HA challenge had no observed effect on the level of BALF total protein (*p<0.05, vs. FA exposed group, N = 5).

Ozone-exposed mice demonstrated increased neutrophil cell counts in BALF when compared to air-exposed animals. Neutrophil recruitment to the airspace was independent of TLR4 (A) and TIRAP (C), but was partially dependent of MyD88 (B) (* p<0.05, vs. FA exposed group; # p<0.05 vs. O₃-WT, N = 4–6 per group).

The level of (A) KC, (B) IL-1β, (C) IL-6, (D) MCP-1 and (E) TNFα in BALF from air and ozone-exposed WT, TLR4−/−, MyD88−/− and TIRAP−/− mice were measured by luminex beads (*p<0.05, vs. FA exposed group; #p<0.05, vs. O₃-exposed group comparisons between strains; N = 4–5 per group).

Animals were exposed to filtered air (FA) or 1 ppm of ozone for 3 hours. Airway responsiveness to methacholine challenge was measured 24 h later. A) Ozone-induced AHR was increased in WT mice but not in TLR4−/− mice, B) MyD88−/−mice, or C) TIRAP−/− mice (*p<0.05 vs. FA-WT; #p<0.05 vs. O3-WT, N = 5–6 per group).

The level of (A) KC, (B) IL-1β, (C) IL-6, (D) MCP-1 and (E) TNFα in BALF from vehicle or HA-challenged WT, TLR4−/−, MyD88−/− and TIRAP−/− mice were measured by luminex beads (*p<0.05, vs. FA exposed group; #: p<0.05, vs. O₃-exposed group comparisons between strains; N = 4 per group).