(A) Mice were sensitized with OVA/alum and exposed to OVA in the presence of vehicle or cTXA₂ and/or ISAP (delivered by osmotic minipumps) as indicated. (B) Total cell number and cell differentials in BALF were analyzed 48 hours after the last airway OVA exposure. n = 6 per group, *P < 0.05. (C) H&E-stained lung sections from vehicle- and cTXA₂-treated mice after OVA sensitization/exposure. Scale bars: 100 μm. Images are shown at original magnification ×40. (D) Scoring of lung sections revealed decreased inflammation in lungs from cTXA₂-treated mice compared with vehicle-treated controls. n = 6 per group, *P < 0.05. Note that the lack of an error bar in the vehicle group is because all vehicle-treated lungs received a score of 3, i.e., 30%–50% of the lung involved in inflammation. (E) IL-9⁺CD4⁺ T cells, as a percentage of CD4⁺ cells in the lung and BALF after OVA-induced allergic lung inflammation. n = 12–13 mice per group, *P < 0.05. (F and G) Th9 cells in mouse lung tissue sections were visualized by immunofluorescence staining using anti–IL-9, anti–IL-10, and anti-CD4 antibodies. Quantitation of the number of IL-9⁺IL-10⁺CD4⁺ T cells per high-power field (HPF). (F) and representative ×40 images (G). n = 7 lungs per group, 5 HPFs per lung, *P < 0.05. Images are shown at original magnification ×40. (H) Airway resistance (R) to increasing doses of methacholine (MCH; left) and at the 25 mg/mL MCH dose (right) of non-allergic mice (vehicle) and OVA-sensitized/exposed mice treated with either vehicle, cTXA₂, cTXA₂+ISAP, or ISAP alone. n = 15–20 per group, *P < 0.05 vs. non-allergic (vehicle), ^#P < 0.05 vs. OVA-sensitized/exposed cTXA₂-treated mice. Significance was evaluated by multiple t tests for B, t test for D–F, and 1-way ANOVA for H.