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. Author manuscript; available in PMC: 2015 Feb 15.
Published in final edited form as: J Immunol. 2014 Jul 11;193(4):1549–1559. doi: 10.4049/jimmunol.1302984

Figure 7.

Figure 7

IL-33 and TSLP play significant roles in type 2 cytokine production and the development of airway hyperreactivity in response to chronic allergen exposure. (A, B, and C) Naïve wild-type mice or mice deficient in cytokine receptors were exposed to allergens as in Figure 6. The lung levels of IL-4 (A), IL-5 (B) or IL-13 (C) were analyzed. Results are the mean ± SEM (n=5 in each group) and are representative of two independent experiments. *: p<0.05, **: p<0.01, compared to wild-type mice. (D through F) Naïve wild-type mice or mice deficient in cytokine receptors were exposed i.n. to PBS or allergens (OAAH) for 4 weeks. Airway reactivity to inhaled methacholine was analyzed as described in the Materials and Methods. (D) The dose response to methacholine in wild-type Balb/c mice as examined by whole body plethysmography is presented. Results are the mean ± SEM (n=20 in each group, a pool of 4 experiments). *: p<0.05, compared to mice exposed to PBS. (E) The dose response to methacholine in wild-type Balb/c mice as examined by a forced oscillation technique is presented. Results are the mean ± SEM (n=5 in each group). *: p<0.05, compared to mice exposed to PBS. (F) Airway reactivity to 6 mg/ml methacholine is presented. Results are the mean ± SEM (n=5 in each group). *: p<0.05, between the groups indicated by horizontal lines.