Objective: To assess the effect of intratracheally administered IL-12 recombinant adenovirus (Adm IL-12) on ovalbumin (OVA) induced bronchial hyperresponsiveness in mouse model.
Methods: C57BL/6 mice were sensitized by ovalbumin. Adm IL-12 with the dose of 10(8)pfu/mouse was administered intratracheally before OVA challenge. IL-4, IL-5 and IFN-gamma in BALF, bronchial responsiveness, eosinophil count in peripheral blood and BALF, serum total IgE and specific IgE were measured.
Results: There was IL-12 gene expression in the lung tissue after Adm IL-12 administration, concentration of IL-12 in sera and BALF were (540 +/- 60) U/ml and (4 700 +/- 800) U/ml respectively, but were unable to be detected in control group (P < 0.01). Compared with the control group, there were significantly lower levels of IL-4 [(3.5 +/- 2.0) ng/ml vs (85.0 +/- 25.0) ng/ml] (t = 27.97, P < 0.01) and IL-5 [(6.5 +/- 4.5) ng/ml vs (54.0 +/- 14.0) ng/ml], (t = 7.92, P < 0.01) in BALF, accompanying with a higher level of IFN-gamma [(690.0 +/- 32.0) ng/ml vs (12.5 +/- 3.2) ng/ml] (t = 51.6, P < 0.01), lower airway resistance [(360 +/- 30) cm H(2)O vs (810 +/- 50) cm H(2)O] (t = 18.9, P < 0.01) and lower eosinophil counts in both peripheral blood [(0.7 +/- 0.1)% vs (9.2 +/- 0.5)%] (t = 47.1, P < 0.01) and in BALF [(3.5 +/- 0.7) x 10(4)/ml vs (21.6 +/- 4.7) x 10(4)/ml)] (t = 9.33, P < 0.01). However, neither serum total IgE [(65 +/- 9) microgram/ml vs (67 +/- 10) microgram/ml], nor specific IgE [(32 +/- 8) microgram/ml vs (33 +/- 8) microgram/ml] showed significant difference (all P > 0.05).
Conclusions: Intratracheally administered Adm IL-12 inhibits ovalbumin induced airway hyperresponsiveness, which may be an effective approach in the management of antigen induced bronchial asthma.