The Changes Of Dendritic Cell In Chronic Obstructive Pulmonary Disease Lung And Its Significance

Chronic obstructive pulmonary disease (COPD) is a frequent disease of respiratory system. With the development of social industrialization and atmospheric pollution, the global disease incidence is rising gradually. However, the pathogenesis of COPD have not yet clarified, Currently that may be related to the chronic airway inflammation,protease and antiprotease imbalance,oxidation and antioxidant imbalance mechanisms, In which Chronic airway inflammation mechanism was concerned. Dendritic cells (Dendritic Cell, DCs) as the most powerful ever found antigen-presenting cells, airway dendritic cells are key regulators of pulmonary immune responses. They can recognize, process, migrate to regional draining pulmonary lymph node and present the processed antigen to naive lymphocytes, and decided what kind of immune response (Thl type, Th2-type or immune tolerance) to complete a "combat mission", played a respiratory tract "sentinel" role.We assume that the airway in COPD patients with such chronic non-specific inflammation and airway and lung parenchyma of DCs dysfunction is closely related to? Therefore, in this experimeniation we can observe the function and number alteration of DCs in the COPD rat models.Objective:Through study function and number alteration of DCs in the COPD will help us to more understanding the role of DCs in chronic non-specific inflammation, but also help to provide the evidence of clarify the pathogenesis of COPD.Mthods:1. Forty normal male SD rats, body weight (200±20) g, were divided into 4 groups randomly and averagely, were called:①Normal cntrol group (I group); ②Smoking 30 days group(Ⅱgroup);③Smoking 60 days group(Ⅲgroup);④Smoking 90 days group (Ⅳgroup); smoking group were placed in home-made smoke box, and lit the cigarette in the box, each time lit two cigarettes, burning for 10 minutes, rest 5 minutes and then placed in another two cigarettes, Smoke 40 cigarettes per day, six days a week.The rat were sacrificed in 30 days,60 days,90 days, Separated the lung tisse and Placed in 4% formaldehyde fixative, routine paraffin embedding, sections 4μm, histological examination (HE and Masson staining) and spared for immunohistochemical. Application of immunohistochemical staining and computer image analysis method of analysis, and to compare the changes of DC distribution number and surface molecules CD80, CD86, MHCⅡin each group.Results:1,COPD group and smoking group expressed lassitude, hair tarn, and locomotor activity declining, coughing, increasing of excretionin respiratory passage. HE staining expressed the character pathobiology changer of COPD.2,There is a increase in DCs number in lungs of COPD model group rats compared with the control group rats(p<0.05), As the longer smoke, the number increased more significantly.3,The expression of costimulatory molecules(CD80,MHC—Ⅱ) was down-regulated in COPD model group compared with the control group rats(p<0.05), As the longer smoke, the down-regulated more significantly.4,The expression of costimulatory molecule CD86 was no difference in COPD model group compared with the control group rats(p>0.05).Conclusions:1,There is an increase in DCs number in lungs of smoking COPD model rat, suggest DCs may be involved in the pathogenesis of COPD.2,The expression of costimulatory molecules(CD80,MHC—Ⅱ) was down-regulated in COPD model rat, suggest COPD rats may be immune dysfunction.