A Study Of The Link Between Imbalanced T-cell-specific Transcription Factors T-bet And GATA-3 And Inflammation Of Upper And Lower Respiratory Passage

Objective To investigate the imbalance of T-cell-specific transcription factorsT-bet and GATA-3 in rats with allergic rhinitis or asthma. And analyze the role of these two transcription factors in the progression of allergic rhinitis and asthma. To observe how these above two factors may be the same mechanism of these two disease. And this may provide the new perspectives for systemic treatment.Method1 Constructing the experimental allergic rhinitis(AR) and asthmatic rats. Rats were immunized by an intraperitoneal injection taking advantage of ovalbumin(OVA) as an antigen and AL(OH)₃ as adjuvants. The AR group was challenged with intranasal instillation; and the asthma group with OVA atomization inhalation. After this progression, these models were detected by action observation and HE staining.2 Getting the blood preparation and dissociating the lymphocyte. The expression levels of T-bet mRNA and GATA-3 mRNA in models were detected by RT-PCR, and analyzed by utilization of statistic methods.ResultsOVA sensitized rats after challenged showed the significant symptom of AR and asthma. And eosinophil infiltration into nasal mucosa of both groups, but control group showed no eosinophil infiltration. This phenomenon in lung was not the same, as it was higher in asthmatic models than those in the other two groups. This demonstrated that the animal experimental models have been constructed successfully.The expression of GATA-3 mRNA in model group was higher than that in the normal group(P<0.05). And it had no significant difference compared with the front group. There was a low expression or no expression in model group, but a higher expression in normal(P<0.05) . The expression between two model groups has no significant difference.ConclusionAllergic rhinitis and asthma models were established successfully. T-bet mRNA and GATA-3 mRNA have unbalanced expression, and this may be the same mechanism of these two disease. Re-establish this balance may provide new perspectives for systemic treatment of allergic airway disease.