A Retrospection On Diagnosis And Treatment The Function Of Molecules In Idiopathic Interstitial Pneumonia

Idiopathic interstitial pneumonia(IIP),or,Idiopathic pulmonary fibrosis(IPF),IIP may therefore be attributable to changes in epithelial morphology and severe damage of the lung tissue accompanying more inflammatory cell accumulation as well as fibrosis and destruction.IIP contain not only interstitial tissue but also epithelial cells,endothelial cells and alveolar.Because alveolar bronchoalveolar fribrosis leads to lung acclimation and total lung capacity reduced. in addition Brochoalveolar infiltrate and pulmonary blood choked bring on hypoxemia and respiratory failure.Pulmonary interstitial disease is relative to immunity system included AM T cells and neutrophils. Those stabled a complex signal network. These signal only express instantly in lung tissue induce a progression fibrosis process. These cycokine is important to "cross talking".Someone thinks fibrosis is the result that extracellular matrix abnormity .In order to search new the rapecetic strategies study the relationship in middle of IL-1,IL-8,TGF-β,MMP-2, MT1-MMP,TIMP-2 in IIP. Hospital records of 105 consecutive patients with pulmonany fibrosis between 1990 and 2002 analyzed the clinical pathological features and the expression of IL-1,IL-8,TGF-β,MMP-2, MT1-MMP,TIMP-2 in mice lung tissue in different period were quantitatively analyzed by RT-PCR in 40 cases of IIP.Result 1, (1)Usual interstitial fibrosing diseases(UIP)occurred more in male (male:female 78:73).The patients'average age 56 years . Pathological features showed bibasal reticular discrepancy abnormalities accompanying fibroblast foci UIP showeded worse reponse to glucocorticoid therapy in pulmonary function, but the clinical manifestation such as progressive dyspnea ,cough and sputum is better than the control team. Acute interstitial pneunoia(AIP) display progressive dyspnoea . Pathological feature is infiltrate.Non-specific interstitial pneumonia(NSIP)showed bibasal uniformitarian pattern. Little of fibrosising pattern. NSIP showeded better response to glucocorticoid therapy than the control team. Pulmonary function is significane 2,The function of molecules in idiopathic interstitial pneumonia .(1)Expression of IL-1 in lung tissue was sifnificantly higher than that of normal controls (t=13.16,p P< 0.01)in first day.After two weeks Expression of IL-1 was substracted .(2) Expression of IL-8 in lung tissue was sifnificantly higher than that of normal controls (t=10.67,P< 0.01).(3) Expression of TGF in lung tissue was sifnificantly three times than that of normal controls (t=13.16, P< 0.01)in third day. During second week TGF was reduced but third week throw out in high level.(4) Expression of MT1-MMP in lung tissue was sifnificantly higher than that of normal controls (t=20.28,P< 0.01).(5)Expression of MMP-2 in lung tissue was sifnificantly higher than that of normal controls (t=12.66,P< 0.01).In fourthly week declined.Conclusions (1)Infection and immunity are diploid that result in IIP.(2)Fibroblst foci and honeycombing exist in the different time which was important UIP features. The histologic patterns of NSIP correlated closely with the therapeutic effect of glucocorticoids. (3)In early IL-1,IL-8,TGF-β excreted stimulated MMP-2,MT1-MMP,TIMP-2 increased. MMP-2 was higher expression which was start-up factor of IIP. MT1-MMP excess expression induced MMP-2 secreted. MMP-2 and TIMP-2 lost blance that conduced IIP aggravated.