[The effects of interleukin-12 inhalation on airway inflammation and T helper cell subsets in mouse asthma models].

OBJECTIVE: To observe the effects of aerosol interleukin-12 (IL-12) on the antigen-induced airway inflammation and T helper cell subsets in mouse asthma models.

METHODS: Thirty BALB/c mice were divided into 3 groups, ten in each group. The mouse asthma models (asthma group) were established by sensitization and challenge with ovalbumin (OVA). One part of sensitized BALB/c mice (IL-12 group) were interfered with aerosol IL-12 from the beginning of sensitization to the end of challenge. The healthy control mice were (control group) treated with normal saline instead of OVA. Broncho-alveolar lavage fluid (BALF) and spleen mononuclear cells (SMNCs) were collected 24h after the last challenge. The total cell numbers and eosinophils (Eos) of BALF were counted. The levels of interferon-gamma (IFN-gamma) and IL-4 of BALF supernatant were measured by ELISA. The mRNA expressions of IFN-gamma and IL-4 in SMNCs were examined by reverse transcript-polymerase chain reaction.

RESULTS: (1) The total cell counts and Eos counts in asthma group [(12.10 +/- 2.23) x 10(9)/L and (2.02 +/- 0.85) x 10(9)/L, respectively] were significantly increased than those in control group [(6.17 +/- 1.34) x 10(9)/L and (0.05 +/- 0.01) x 10(9)/L, respectively] (P < 0.01), while in IL-12 group the above counts [(8.41 +/- 1.71) x 10(9)/L and (0.15 +/- 0.08) x 10(9)/L, respectively] were significantly decreased than those of asthma group (P < 0.05). (2) The IFN-gamma and IL-4 levels of BALF supernatant in asthma group [(43.60 +/- 15.60) ng/L and (27.15 +/- 10.42) ng/L] had significant differences from those in control group [(83.76 +/- 19.02) ng/L and (0.84 +/- 0.69) ng/L, respectively] (P < 0.01) and from those in IL-12 group [(62.30 +/- 12.50) ng/L and (6.22 +/- 2.28) ng/L, respectively](P < 0.01). (3) The IFN-gamma and IL-4 mRNA expression of SMNCs in asthma group (0.64 +/- 0.14 and 0.89 +/- 0.31), respectively) had significant differences from those in control group (1.18 +/- 0.34 and 0.71 +/- 0.16, respectively) (P < 0.05) and those in IL-12 group (0.89 +/- 0.26 and 0.79 +/- 0.25, respectively) (P < 0.05) as well.

CONCLUSION: The experiment data suggested that IL-12 aerosol inhalation might inhibit antigen-induced airway inflammation and partly reverse the deviation of Th cell subsets in mouse asthma models.