The Method Of The Warm Sputum Inhaus Effect On The Immunoregulation Of The Non-eosinophilicasthma

Obeject Through to examination TLR3 in dendritic ,NF- kB in peripheral blood mononuclear cell and IL-6, the IL-8 level in the blood plasma cell in the eosinophilic asthma, the non- eosinophilic asthma and the ordinary viral cold respective,as well as the non- eosinophilic asthma pathogenesis which induced to the viral infection, induced the factor and treated the function mechanism observation to the warm sputum inhaust Chinese native medicine which the noneosinophilic asthma acute manifests suddenly. Discusses relations whichTLR3, NF- kappa B, IL-6, IL-8 and the non- eosinophilic asthma arised,and the treatment of the warm sputum inhaust effect on the immunoregulation of the non- eosinophilicasthma exeactly.Methods By the induction phlegm inspection, divides into the asthma patient ,the eosinophilic asthma group (B group) 30 person and the non- eosinophilic asthma (C group) 100 people, simultaneously the ordinary cold compares the group (A group) 30 people.The noneosinophilic asthma patient stochastically divided into the comparison group (the C1 group) and the experimental group (the C2group), each group of 50 people. Blood drawed from the vein who have empty stomach, examined TLR3 in dendritic with the RT-PCR ,NF- kB in peripheral blood mononuclear cell In EMSA and IL-6, the IL-8 level in the blood plasma cell by ELISA, and intervened by the warm phlegm inhaust law its around. Experimental group: Gave the inspiration β2 receptor agonist + inspiration glucocorticoid + antibiotic + warm phlegm inhaust treatment; Comparison group: Gave the inspiration β2 receptor agonist + warm phlegm inhaust treatment + antibiotic treatment; eosinophilic cell asthma group: Gave the inspiration β2 receptor agonist +inspiration glucocorticoid + antibiotic treatment; Normal comparison group: The virulent cold patient, accepts the conventional treatment.Results1. the normal comparison group,TLR3, NF- kB,. IL-6 and the IL-8level of patient is lowe.2. In the non- eosinophilic asthma group, TLR3 , NF- kB, IL-6 and theIL-8 level of patient, the experimental group remarkably is lower than the comparison group.3. Eosinophilic asthma group and non- eosinophilic asthma group's comparison group, in inspection TLR3 in dendritic ,NF- kB in peripheral blood mononuclear cell and IL-6, the IL-8 level in the blood plasma cell , two groups of between differences not remarkable significances (P > 0.05).4. The eosinophilic asthma group, the non- eosinophilic asthma group's comparison component compare with the normal comparison group respective, TLR3, NF- kB, the IL-6 IL-8 level is remarkably higher than the normal comparison group (P <0.05).Conclusion After the viral infection duplicates produces dsRNA, through with the TLR3 union, and promotes its expression, activates NF-kB, surrendered IL-6 and the IL-8 level in the blood plasma, subsequently promotes neutrophilic granulocyte to infiltrate in trachea, this way causes the non- eosinophilic asthma acute episode. Heavy breathing sickness is belongs phlegm inhaust getssick "to bend down drinks" the card. The warm phlegm inhaust law might through suppress the non- eosinophilic asthma a series of immune response, with the inspiration glucocorticoid, the receptor agonist and so on the commonly used medicine by drug combination can effectively control the asthma to acute episode...