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Asthma, a respiratory disease, is notably characterized by reversible airway obstruction, persistent lung inflammation, and airway hyperresponsiveness (AHR). Nasal insufflation of IL-11 causes AHR in wild-type mice while lung inflammation induced by antigen sensitization and challenge, which mimics features of atopic asthma in humans, is attenuated in mice genetically deficient in IL-11 receptor subunit \u03b1-1 (IL-11R\u03b11-deficient mice), a transmembrane receptor that is required conjointly with glycoprotein 130 to transduce IL-11 signaling. Nevertheless, the contribution of IL-11R\u03b11 to characteristics of nonatopic asthma is unknown. Thus, based on the aforementioned observations, we hypothesized that genetic deficiency of IL-11R\u03b11 attenuates lung inflammation and increases airway responsiveness after acute inhalation exposure to ozone (O<jats:sub>3<\/jats:sub>), a criteria pollutant and nonatopic asthma stimulus. Accordingly, 4 and\/or 24 h after cessation of exposure to filtered room air or O<jats:sub>3<\/jats:sub>, we assessed lung inflammation and airway responsiveness in wild-type and IL-11R\u03b11-deficient mice. With the exception of bronchoalveolar lavage macrophages and adiponectin, which were significantly increased and decreased, respectively, in O<jats:sub>3<\/jats:sub>-exposed IL-11R\u03b11-deficient as compared with O<jats:sub>3<\/jats:sub>-exposed wild-type mice, no other genotype-related differences in lung inflammation indices that we quantified were observed in O<jats:sub>3<\/jats:sub>-exposed mice. However, airway responsiveness to acetyl-\u03b2-methylcholine chloride (methacholine) was significantly diminished in IL-11R\u03b11-deficient as compared with wild-type mice after O<jats:sub>3<\/jats:sub>exposure. 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