The Significance Of LIGHT Expression In The Lungs Of Mice Pulmonary Fibrosis Models

Interstitial lung disease (ILD) is a kind of severe diseases that pulmonaryinterstitium, alveoli and bronchioles are mainly involved in. The commonsyndromes are gradual dyspnea, restricted ventilation function disturbance anddiffusion function (Dlco) degradation, hyoxemia and diffuse procession in theimageology. It will develop to be diffuse pulmonary fibrosis, honeycomb lung,and eventually to be respiratory failure. It includes 180 categories of diseases.Idiopathic pulmonary fibrosis (IPF) is the most common one. Thepathogenesis of IPF is still unknown. We use silicon dioxide to make themodel of mice pulmonary fibrosis to detect the pathogenesis.Objective: We use silicon dioxide to make the model of mice pulmonaryfibrosis and use the RT-PCR method to detect the variance of the expression ofLIGHT gene.Method: We use 84 mice to make the models of pulmonary fibrosis andthe controls. The amount of the models of pulmonary fibrosis and the controlsare equal. Silicon dioxide suspension (200mg/kg) intro-trachea perfuse tomake the model of mice pulmonary fibrosis. Execute the mice in both groupsin 3 days (Group 1), 7 days (Group 2), 2 weeks (Group 3), 4 weeks (Group 4),8 weeks (Group 5), 12 weeks (Group 6), 16 weeks (Group 7), and there are sixmice in the models and the controls each group. Obtain the left lungs and thespleens and extract the total mRNA. Using the RT-PCR method, we detectwhether there are variance in the expression of LIGHT. We use the right lungsto detect the pathology.Result: (1) Pathology: â‘ We can see normal pulmonary architecture inthe controls. â‘¡We see inflammatory cells infiltration in the pulmonaryinterstitium, the alveoli becoming detelectasis, the alveolar septums becomingwider, more and more collagen deposition and fibroblast proliferation in theGroup 1 to Group7. The inflammatory cells are macrophages andlymphocytes. The amount of the lymphocytes are increased in the early periodof inflammation and decreased in the other period of inflammation. But wedon't find typical cellular and fibrous tubercles in all groups. To obtain thetypical pulmonary fibrosis, we must wait more time. (2) RT-PCR: Theexpressions of LIGHT are obviously increased in the early 7days (all in Group1 and part in Group 2) in both lungs and spleens, and LIGHT expressions arenot detected in the lungs at the development ages of the model groups (Group3 to Group 7) and all of the control groups. There are significant differencesbetween model group1 and the control group 1 in the spleens (P<0.05). Thereare no differences in the spleens of other model groups (Group 2 to Group 7)and all of the control groups themselves. Conclusion: The method of using silicon dioxide to make the model ofmice pulmonary fibrosis is simple, reliable and the progression is torpidity.The pathology is similar to most species of ILD, such as IPF. The expressionof LIGHT is highly raised up in the early when the inflammation is developing.It may play a significant role in the early promotion of inflammations, theearly injury of lungs and let the inflammations go on. The inflammations andinjuries march in turn, which make the necessity for the fibrosis. In theprogress of the pulmonary fibrosis, we don't find out the high expression ofLIGHT, the subtype of lymphocytes must lead to the Th2 group and Th2cytokines are more predominant than Th1 cytokines, and they are benefit tofibrosis. In the normal condition, there is slightly expression in the spleens,which mustn't cause pneumonia or pulmonary fibrosis.