Objective: To investigate the effect of a mouse IL-12 gene expressive plasmid (mIL-12 plasmid) on the airway inflammation and the cytokine production in asthmatic mice and to study the possible mechanisms.
Methods: A mouse model of asthma was established by sensitization with ovalbumin (OVA). Forty-one BALB/c mice were divided into six groups including an asthmatic model group (group A, eight mice, sensitized with OVA plus challenging with OVA by aerosol), a model control group (group B, six mice, sensitized with OVA plus aerosolizing with normal saline), a mIL-12 plasmid prevention group (group C, eight mice, receiving intramuscularly mIL-12 plasmid 100 micro g on day 1, day 3, and day 5), a mIL-12 plasmid treatment group (group D, eight mice, receiving intramuscularly mIL-12 plasmid 100 micro g on day 14, day 16, and day 18), an empty plasmid prevention group (group E, five mice, receiving intramuscularly empty plasmid 100 micro g on day 1, day 3, and day 5), and an empty plasmid treatment group (group F, six mice, receiving intramuscularly empty plasmid 100 micro g on day 14, day 16 and day 18). The number of EOS and the concentration of IL-4, IL-5 and IFN-gamma in the mouse bronchoalveolar lavage fluids (BALF) were detected.
Results: The number of EOS and the concentration of IL-4, IL-5 and IFN-gamma from group B were (0.01 +/- 0.03) x 10(8)/L, (24 +/- 4) pg/ml, (33 +/- 6) pg/ml, (725 +/- 59) pg/ml,respectively; those from group C were (0.06 +/- 0.04) x 10(8)/L, (43 +/- 13) pg/ml, (63 +/- 10) pg/ml, (626 +/- 60) pg/ml, respectively, and those from group D were (0.11 +/- 0.12) x 10(8)/L, (38 +/- 14) pg/ml, (66 +/- 14) pg/ml, (661 +/- 40) pg/ml, respectively; the difference was significant as compared with those from group A [(2.97 +/- 1.20) x 10(8)/L, (122 +/- 45) pg/ml, (126 +/- 34) pg/ml, and (435 +/- 49) pg/ml] (P < 0.001). The number of EOS and the concentration of IL-4, IL-5 and IFN-gamma from group C and group D also showed significant difference in comparison with those from group E [(1.96 +/- 0.93) x 10(8)/L, (110 +/- 24) pg/ml, (112 +/- 11) pg/ml and (464 +/- 51) pg/ml], and group F [(2.11 +/- 0.90) x 10(8)/L, (88 +/- 17) pg/ml, (107 +/- 6) pg/ml and (481 +/- 64) pg/ml] (P < 0.01).
Conclusion: The mIL-12 plasmid can significantly inhibit airway inflammation. Its regulatory effect on the balancing of Th1/Th2 cytokines may be a possible mechanism.
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