Inflammatory cells and T lymphocytes in bronchoalveolar lavage fluid from asthmatic patients: Relationship with development of asthmatic symptoms and therapeutic responese / 알레르기

OBJECTIVES: Chronic asthma has a number of characteristic feature; the increased airway responsiveness and bronchial inflammation. Although these mechanisms are not clear, activated T-cell has had an important role in migration and activation of inflammatory cells. In order to evaluate the role of T-lymphocyte and T-cell subsets in the development of asthmatic symptoms and the posibility for predicting the therapeutic response, we performed bronchoalveolar lavage from asymptomatic and symptomatic asthmatic subjects and inflammatory cell count, T-cell subset, activated T-lymphocyte were analysed and they were compared with healthy controls. METHOD: 76 bronchial asthmatics and 54 healthy controls were enrolled in this study. Asthmatic patients were classified into symptomatic and asymptomatic group according to symptom severity. Symptomatic group was divided into two groups according to therapeutic response ; early responder(ER) and late responder(LR). Lymphocytes(T-lymphocytes subsets and activation marker) in bronchoalveolar lavage(BAL) cells were analyzed using a flow-cytometry. RESULTS: The counts of eosinophil and neutrophil in BAL fluid were significantly higher in both asymptomatic and symptomatic asthmatic patient than those of healthy controls (p0.05), the numbers of T3 and T4 lymphocyte subsets were significantly higher in LR than in healthy controls, and the number of T3-IL2R+, T4-IL2R+ lymphocytes were significantly higher in ER than in healthy controls(p<0.05). CONCLUSION: We could conclude that the infiltration and activation of T-lymphocytes might be associated with the development of asthmatic symptoms and responsiveness to therapy.

A Study of EFFECT and MECHANISM of IL-2on SURVIVAL of EOSINOPHILS / 결핵

BACKGROUND: Interleukin-5 (IL-5) is responsible for eosinophilia in allergic diseases. In allergic bronchial asthma, there is a correlation between the extent of eosinophil infiltration in bronchial mucosa and IL-5 concentrations. In addition, IL-2 concentration is elevated in the airways and associated with eosinophilia in symptomatic patients with bronchial asthma. In animal studies, IL-2 can induce eosinophilia by increasing the synthesis of IL-5, however, it is still unknown how IL-2 can induce eosinophila in human being. The aim of this study is to evaluation the effect and mechanism of IL-2 on prolongation of eosinophil survival. METHODS: After purifiing the eosinophils from the venous blood of allergic patients with eosinophilia, we measured the survival rates of eosinophils using trypan blue dye exclusion test, and the number of eosinophils with Randolp's solution. We compared the survival rates of eosinophils in the presence of IL-2 or IL-5. Neutralizing antibody for IL-5 was added in IL-2 treated eosinophils to reveal whether IL-2 induced prolongation of eosinophil survival was mediated by IL-5. We checked IL-5 m-RNA expression of lymphocytes in the presence of IL-2 by using Reverse transcription-Polymerase chain reaction (RT-PCR) method to revealed the effect of IL-2 on IL-5 m-RNA expression on lymphocyte. alpha and beta IL-2 receptors were measured on eosinophils and lymphocytes with flow-cytometer after stimulated with IL-2. RESULTS: 1) Eosinophil survival rates increased dose dependently on IL-5 and IL-2. 2) The eosinophil survival rates increased by IL-2 were not inhibited by the pretreatment with neutralizing antibody for IL-5. 3) IL-5 m-RNA was not expressed on lymphocytes by the treatment with IL-2 up to 96 hours. 4) IL-2 upregulate the expression of IL-2Ralpha on eosinophils, instead of no effect on the expression of IL-2Rbeta. CONCLUSION: Interleukin-2 had the enhancing effect on the survival rates of eosinophils. The mechanism behind IL-2 induced eosinophilia might be the increment of IL-2 receptors on eosinophils rather than IL-5 synthesis by lymphocytes.