[A study on the roles of CD86 in antigen-induced eosinophil infiltration into airways and airway hyperresponsiveness]

To explore the effect of CD86 on antigen-induced eosinophil infiltration into the airways and airway hyperresponsiveness in sensitized mice, and further elucidate the role of CD86 in the pathogenesis of bronchial asthma.

Female BALB/c mice (n = 8 for each group) were sensitized and challenged with ovalbumin to induce airway eosinophilia and airway hyperresponsiveness. Airway responsiveness was espressed by the provocative concentration of acetylcholine causing 50% increase in respiratory resistance (PC50). Effect of anti-CD86 monoclonal antibody (mAb) on antigen-induced changes of eosinophil numbers in brochoalveolar lavage fluid (BALF) and airway reactivity was observed. CD86 expression on BALF cells was detected by flow cytometry and concentrations of interleukin-4 and interleukin-5 in homogenized supernatant of lung tissue were determined by ELISA.

In sensitized mice challenged with ovalbumin 20 minutes once a day for 6 days, the number of BALF eosinophils was (9.2 +/- 1.5) x 10(8)/L. However, no eosinophil could be found in the BALF from mice without ovalbumin sensitization and challenge. Also, ovalbumin treatment led to PC50 value decrease from (0.66 +/- 0.13) g/L to (0.17 +/- 0.07) g/L (P < 0.01). CD86 expression on BALF cells from ovalbumin sensitized- and challenged-mice (36.4 +/- 6.2) was much higher than that from control mice (12.3 +/- 3.6, P < 0.01). In mice treated with intravenous injection of anti-CD86 mAb before each challenge, BALF eosinophils decreased by 67% (P < 0.01), and PC50 value increased by 69% (P < 0.01). Our results showed that anti-CD86 mAb prevented antigen-induced airway eosinophilia and airway hyperresponsiveness accompanied by a decrement of levels of both interleukin-4 and interleukin-5 in lung tissue.

Anti-CD86 mAb is able to inhibit antigen-induced airway eosinophilia and to ameliorate airway hyperresponsiveness, possibly by inhibiting production of interleukin-4 and interleukin-5. These data suggested that the blockade of airway antigen-presenting cells' functions couid be of value in treatment of human asthma.