RationaleIL-13 is a central cytokine in allergic inflammation and asthma. It mediates its effects through the heterodimeric IL-4Rα/IL-13Rα1 complex. IL-13Rα2 has been postulated to be a decoy receptor, because it binds IL-13 with high affinity, yet does not lead to signaling through the Jak-Stat pathway. Since overexpression of IL-13Rα2 has been shown to inhibit IL-13 responses, we hypothesized that the differences in airway hyper-responsiveness (AHR) observed among the various strains used in murine models of asthma may be due to variations in serum IL-13Rα2 prior to sensitization.MethodsBALB/c, A/J, FVB/n, C3H/Hej, and C57BL/6 mice (n = 4-5) were kept in specific pathogen free conditions. Blood was obtained from the lateral tail veins of mice. ELISA was used to measure IL-13Rα2 protein in mouse serum.ResultsBALB/c and A/J mice, which have been reported to have increased AHR compared to the other mouse strains, had 10.3 ng/ml and 14.3 ng/ml of serum IL-13Rα2, respectively. These levels were significantly lower than that of FVB/n (20.3 ng/ml; p < 0.03), C3H/Hej (22.6 ng/ml; p < 0.04), and C57BL/6 (19.9 ng/ml; p < 0.02), strains that develop less AHR after allergen challenge.ConclusionsSerum IL-13Rα2 protein at baseline is inversely correlated with the previously published reports of strain specific AHR in murine asthma models. This suggests that circulating IL-13Rα2 may be one factor in determining the propensity for or severity of atopic asthma. RationaleIL-13 is a central cytokine in allergic inflammation and asthma. It mediates its effects through the heterodimeric IL-4Rα/IL-13Rα1 complex. IL-13Rα2 has been postulated to be a decoy receptor, because it binds IL-13 with high affinity, yet does not lead to signaling through the Jak-Stat pathway. Since overexpression of IL-13Rα2 has been shown to inhibit IL-13 responses, we hypothesized that the differences in airway hyper-responsiveness (AHR) observed among the various strains used in murine models of asthma may be due to variations in serum IL-13Rα2 prior to sensitization. IL-13 is a central cytokine in allergic inflammation and asthma. It mediates its effects through the heterodimeric IL-4Rα/IL-13Rα1 complex. IL-13Rα2 has been postulated to be a decoy receptor, because it binds IL-13 with high affinity, yet does not lead to signaling through the Jak-Stat pathway. Since overexpression of IL-13Rα2 has been shown to inhibit IL-13 responses, we hypothesized that the differences in airway hyper-responsiveness (AHR) observed among the various strains used in murine models of asthma may be due to variations in serum IL-13Rα2 prior to sensitization. MethodsBALB/c, A/J, FVB/n, C3H/Hej, and C57BL/6 mice (n = 4-5) were kept in specific pathogen free conditions. Blood was obtained from the lateral tail veins of mice. ELISA was used to measure IL-13Rα2 protein in mouse serum. BALB/c, A/J, FVB/n, C3H/Hej, and C57BL/6 mice (n = 4-5) were kept in specific pathogen free conditions. Blood was obtained from the lateral tail veins of mice. ELISA was used to measure IL-13Rα2 protein in mouse serum. ResultsBALB/c and A/J mice, which have been reported to have increased AHR compared to the other mouse strains, had 10.3 ng/ml and 14.3 ng/ml of serum IL-13Rα2, respectively. These levels were significantly lower than that of FVB/n (20.3 ng/ml; p < 0.03), C3H/Hej (22.6 ng/ml; p < 0.04), and C57BL/6 (19.9 ng/ml; p < 0.02), strains that develop less AHR after allergen challenge. BALB/c and A/J mice, which have been reported to have increased AHR compared to the other mouse strains, had 10.3 ng/ml and 14.3 ng/ml of serum IL-13Rα2, respectively. These levels were significantly lower than that of FVB/n (20.3 ng/ml; p < 0.03), C3H/Hej (22.6 ng/ml; p < 0.04), and C57BL/6 (19.9 ng/ml; p < 0.02), strains that develop less AHR after allergen challenge. ConclusionsSerum IL-13Rα2 protein at baseline is inversely correlated with the previously published reports of strain specific AHR in murine asthma models. This suggests that circulating IL-13Rα2 may be one factor in determining the propensity for or severity of atopic asthma. Serum IL-13Rα2 protein at baseline is inversely correlated with the previously published reports of strain specific AHR in murine asthma models. This suggests that circulating IL-13Rα2 may be one factor in determining the propensity for or severity of atopic asthma.