| Objective: To discuss the level of soluble B7-H3in the peripheral blood of childrenwith bronchial asthma, and analyze its correlation with the expression of cytokines, toexplore the clinical significance of abnormal expression of soluble B7-H3in acute phase ofbronchial asthma.Methods:21cases of children with bronchial asthma were enrolled at department ofrespiration of Children’s hospital affiliated in Soochow university from January2012toDecember2012, and16cases of children (Indirect inguinal hernia, hemangioma, adenoidhypertrophy) hospitalized in surgery as control group children, divided into acute phase ofasthma group (group A), recovery phase group (group B) and control group (group C). Atthe same time, peripheral blood were collected in children with bronchial asthma in acutephase and recovery phase as well as children in surgery, Enzyme-linked immunosorbentassay were used to detect the level of soluble B7-H3, IFN-gamma, interleukin-4andinterleukin-10in plasma, and analyze the correlation between the level of soluble B7-H3and cytokines IFN-gamma, interleukin-4, interleukin-10in plasma in acute phase ofasthma.Results: The level of soluble B7-H3in plasma in acute phase of asthma group weresignificantly higher than the recovery phase group and control group (P<0.05), whilerecovery phase group was higher than control group, but no significant difference, the levelof IFN-gamma and interleukin-10in acute phase of asthma group were lower than that ofrecovery phase group and control group (P<0.05), recovery phase group and control grouphad no significant difference. The level of interleukin-4in plasma both in acute phase ofasthma group and recovery phase group were higher than that of control group (P<0.05),and the level in acute phase of asthma group was higher than that of recovery phase group (P<0.05). The level of soluble B7-H3and the level of interleukin-4in plasma has positivecorrelation in children in acute phase of bronchial asthma, and has no correlation withIFN-gamma, interleukin-10.Conculsion: The level of soluble B7-H3was abnormal high expression in acute phaseof bronchial asthma, soluble B7-H3may enhance the secretion of Th2type cytokines andhas effect in acute phase of bronchial asthma. Objective: To explore the therapeutic function of anti B7-H3monoclonal antibody inmouse model of asthma in induction phase and effector phase.Methods: Female BALB/c mice (weight18-20g and6-8wk old) were divided intofive groups, every group has10mice, asthmatic group (group A), normal saline controlgroup (group B), IgG group (group C), anti B7-H3antibody induction group (group D),anti B7-H3antibody effector group (group E). Mice in group A, group C, group D andgroup E were given OVA sensitization and excitation (mice were sensitized to OVA byintraperitoneal injection on days0and10, then they were exposed to OVA aerosolchallenges for thirty minutes on consecutive seven days on day20), group C and group Dwere given intraperitoneal injection of IgG and anti B7-H3antibody on days2,7,11,14,18, group E were given intraperitoneal injection of IgG on days2,7,11,14,18,intraperitoneal injection of anti B7-H3antibody on days21,24,26(intraperitonealinjection before one hour of OVA challenges). Mice in group B were given saline as abovemethods. After two hour of last challenge all mice were anesthetized to death to collectsamples, all mice were alveolared lavage, and bronchoalveolar lavage fluid (BALF) werecollected to count cells number and classify cells, measure the level of IFN-gamma,interleukin-4, interleukin-17in BALF by Enzyme-linked immunosorbent assay, mouselung tissue sections stained with HE, PAS and immunohistochemical method (SABCmethod), to observe the infiltration of inflammatory cells and eosinophilic cells, mucussecretion and the expression of B7-H3in lung tissue.Results: The total cells and eosinophilic cells in bronchoalveolar lavage fluid inasthmatic group were more than the normal saline control group and anti B7-H3antibody induction group, the difference were statistically significant (P<0.05). The total cells andeosinophilic cells in bronchoalveolar lavage fluid in asthmatic group, IgG group and antiB7-H3antibody effector group were no statistically significant. The total cells andeosinophilic cells in anti B7-H3antibody induction treatment group were more than thenormal saline control group (P<0.05). The level of IFN-gamma in BALF in asthmaticgroup, IgG group, anti B7-H3antibody induction group and anti B7-H3antibody effectorgroup were lower than the normal saline control group (P<0.05), the level of IFN-gammain asthmatic group, IgG group and anti B7-H3antibody effector group were no statisticallysignificant, the level of IFN-gamma in anti B7-H3antibody induction group were higherthan IgG group (P<0.05). The level of interleukin-4and interleukin-17in asthmatic group,IgG group, anti B7-H3antibody induction group and anti B7-H3antibody effector groupwere higher than the normal saline control (P<0.05), the level of interleukin-4,interleukin-17in asthmatic group, IgG group and anti B7-H3antibody effector group wereno statistically significant, the level of interleukin-4, interleukin-17in anti B7-H3antibodyinduction group were lower than IgG group (P<0.05). Lung tissue pathological stainedshowed more infiltration of inflammatory cells, eosinophilic cell and mucus secretion inasthmatic group, IgG group, anti B7-H3antibody effector group than that of anti B7-H3antibody induction group, normal saline control group no significant infiltration ofinflammatory cells, eosinophilic cell and mucus secretion. Immunohistochemistry showedhigh expression of B7-H3in asthmatic group and IgG group, normal saline control groupdid not express B7-H3, and B7-H3partly expression in anti B7-H3antibody inductiongroup and anti B7-H3antibody effector group.Conculsion: Treatment with anti B7-H3monoclonal antibody in induction phase ofasthma can inhibit secretion of Th2type cytokine (interleukin-4) and Th17type cytokines(interleukin-17), and promote secretion of Th1type cytokine (IFN-gamma), there byreducing the airway pathological change of mouse model of asthma induced by OVA. |
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