FIGURE 3.

Lentiviral overexpression of MKP‐1 abrogates Gln deficiency‐induced neutrophilic inflammation. (A–B) Representative immunoblots (A) and immunohistochemical stainings (B) for MKP‐1 protein. Normal mice were injected with varying virus doses and sacrificed 2 days thereafter for western blots (A, n = 9–12, three independent experiments) or immunohistochemistry of the lung (B, n = 6, three independent experiments). The bars indicate 100 μm. C, MKP‐1 and phosphorylation of p38 and cPLA₂ (n = 10–15, three independent experiments) in the lungs of mice pretreated with lentiviral MKP‐1. (D–E) The levels of neutrophils at 10 h (D, n = 15–20, three independent experiments) and Th1 cytokines at 1.5 h (E, n = 15–20, three independent experiments) in BALF. (C–E) GPNA and viruses (4 × 10⁷ IU) were injected 1 h and 2 days before the second airway challenge, respectively. Data are presented as the mean ± SEM. (A) ns p > .05 vs. normal control, *p < .05 vs. normal control, **p < .001 vs. normal control. (C–E) *p < .05 vs. saline control, **p < .001 vs. saline control, #p < .05 vs. OVA group, ##p < .001 vs. OVA group, ns p > .05 vs. OVA + GPNA group, $p < .05 vs. OVA + GPNA group, $$p < .001 vs. OVA + GPNA group. BALF, bronchoalveolar lavage fluid; cPLA₂, cytosolic phospholipase A₂; eGFP, enhanced green fluorescent protein; GAPDH, glyceraldehyde 3‐phosphate dehydrogenase; Gln, glutamine; GPNA, L‐γ‐glutamyl‐p‐nitroanilide; IL, interleukin; MKP‐1, MAPK phosphatase‐1; ns, not significant; OVA, ovalbumin; SEM, standard error of the mean; TNF, tumor necrosis factor