Effects of Gln deficiency on MKP‐1 induction and p38 phosphorylation. (A) Representative immunoblots and densitometric analyses of GS. GS siRNA was injected intravenously from days 7 to 1, and control siRNA was administered at day 5 (n = 6, three independent experiments). (B) Measurement of Gln levels in the lungs using a Gln assay kit. Normal mice were treated either with siRNAs 5 and 3 days before or with GPNA 1 h before sacrifice (n = 12–15, three independent experiments). (C–D) Representative immunoblots and densitometric analyses of the MKP‐1 protein and p38 phosphorylation in the lungs of mice pretreated with GPNA (1 h before the second airway challenge; (C) n = 10–13, three independent experiments) or GS siRNA (5 and 3 days before the second airway challenge; (D) n = 10–13, three independent experiments). Data are presented as the mean ± SEM. A‐B, ns p > .05 vs. normal control, *p < .05 vs. normal control, **p < .01 vs. normal control. (C–D) *p < .05 vs. saline control, **p < .01 vs. saline control, ns p > .05 vs. OVA group, #p < .05 vs. OVA group, ##p < .01 vs. OVA group. GAPDH, glyceraldehyde 3‐phosphate dehydrogenase; Gln, glutamine; GPNA, L‐γ‐glutamyl‐p‐nitroanilide; GS, glutamine synthetase; MKP‐1, MAPK phosphatase‐1; ns, not significant; OVA, ovalbumin; SEM, standard error of the mean; siRNA, small interfering RNA