In order to explore the relationship between xenograft rejection and cytokines, the proliferative responses and cytokine contents from human lymphocyte were detected in porcinehuman mixed lymphocyte culture (MLC) and compared with human allo-MLC. The results showed that the proliferative responses in the former was equal to or stronger than that in the latter, and the kinetics of IL-2 and IFN-Y in both supernatants were similar but the peak of IL-4 from the former was higher than that from the latter (P<0.05). This suggests that cytokines are likely to play roles in porcine-human MLC.

Objective To establish a model of asthma mice with spleen-deficiency syndrome (asthma-SDS) and to investigate the effects of Cryptoporus volvatus ferment substance (CVFS) on the airway hyperresponsiveness and inflammation in model mice. Methods An asthma-SDS model of mice was established by ovalbumin (OVA)-sensitized plus over-eating and over-exerting. The changes of lung resistance (R_L), inflammatory cells in bronchoalveolar lavage fluid (BALF), lung tissue pathology, and spleen index were observed. Results Compared with the simple asthma model of mice, the airway hyperresponsiveness, eosinophils number in the BALF, lung tissue pathology, and spleen index in the asthma-SDS model of mice showed a significant difference (P

Aim Establish a novel mouse model of airway goblet cell hyperplasia and mucus hypersecretion.Method BALB/c mice were sensitized subcutaneously with ovalbumin(OVA) allergens in aluminium hydroxide at d 0,re-sensitized once intraperitoneally d 10 after first sensitization,and challenged with OVA aerosolly daliy from d 15 to d 21 after first sensitization.Inflammatory cell number in BALF,eosinophil infiltration in the lung tissue with HE stain and goblet cells in the bronchial mucous membrane with PAS stain were examined.Dexamethasone was employed to validate the model.Results Mice sensitized and challenged with OVA showed a significantly hyperplasia of goblet cells in the bronchial mucous membrane,increased mucus in the alveolar cavity,eosinophil infiltration in the lung tissue and increased number of inflammatory cells in BALF.Those pathological changes were inhibited by dexamethasone and mIL-2 plasmid.Conclusion This model helps to screen the new drugs for mucus hypersecretion and research on the pathological mechanism of airway mucus hypersecretion.