Specially sending fiber _'s general knowledge of cause of disease of lung

Specially sending fiber _'s general knowledge of cause of disease of lung
Specially the sending fiber cause of disease of lung is not clear. Virus, fungi, environmental pollution, toxic material can be influenced. Have not found yet specially the sending lung fiber has clear hereditary foundations or inclination, there are quite few heredity or families. It sees family the intersection of lung and clinical manifestation that fiber take of taking place etc. specially to be and clinical manifestation of family similar. Though heredity transmit mode expound by mutant and outside apparent to lead, can believe person who send lung fiber turn the dominant heredity of autosome specially yet, special gene on chromosome No. 14 may until lung of sending etc. whom fiber take high to endanger, have something to do specially, leucocyte antigen of person on chromosome No. 6 (HLA) Have nothing to do with specially sending lung fiber.
Specially the sending fiber morbidity of lung may be inflammation, result that tissue damaging, repair superposes continuously. Cause the cause of disease to usually act immune cells on the lung and reside, produce inflammation or immunoreaction, they can also damage upper skin cells or endothelial cells directly.
1,Immunity and inflammation react
Specially sending lung fiber is early may be produced and resisted specific immunoreaction. It is the damage that a lung can be checked initially that inflammation of the lower respiratory tract reacts. Among lymphocyte, macrophage at quality and alveolus is and neutral grains of cell increase. T lymphocyte damaged in specially sending lung fiber lung and played a double role in the regulation of disease progress. Present and activate the state from T lymphocytes that is specially obtained in the sending lung fiber patient's alveolus, can express IL-2 receptor and secrete INF - . The product that T lymphocytes secreted can already be inhibited into the hyperplasia of fibrous cells, can also strengthen into collagen of fibrous cells and formate. In addition T lymphocyte have enormous auxiliary function too to the intersection of B and lymphocyte, this pair strengthen immune production of complex for important very much.
The intersection of lung and to influence to it gathers to be very important inflammatory cell that lung organize specific immunoreactive production under essence. The alternative stick the molecule, sticks the molecule and combines plainly and plays an important role with immunoglobulin (Ig) in the interaction of inflammatory cell and endothelial cell. The sticking firmly of a lot of cells depends on sticking molecule - a (ICAM-1) of cells Leucocyte function antigen of sum - a (LFA-1) . TNF - induces ICAM-1 to express on the surface of endothelial cell. The leucocyte outside the blood vessel includes it is expressed in the leucocyte and junction of endothelial cells that LFA-1 and blood platelet endothelial cell stick the molecule. Fibrinolysin activator (urine kinase u-PA) of urine kinase type It may be a degradation product of protein hydrolase from blood vessel to different tissues in a of sport course of alveolus of inflammatory cell. Specially the sending lung fiber inflammatory cell is moved and relied on many kinds of chemical materials directly. It is plain that the factor of hastening and melting includes lying between in vain - a (IL-1) , the monocyte trends towards and melts albumen - a (MCP-1) , macrophage inflammatory albumens - Ia (MIP-1a) , alexinic composition C5a, cell factor (MCP-1MIP-1a) , fiber connect include, act on RGD, pale 3 alkene B4(LTB4) of macrophage usually , IL-8 and acting on C5a of the leucocyte. T lymphocyte, alveolus macrophage, endothelial cell, at leather for cell, be become whether there are these cells of the sources importants of factor on cells fibrous. Urine kinase receptor (u-PAR, CD87) It is the essential trending towards the factor of melting to monocyte and PMN. U-PAR may influence the leucocyte to circulate and activate the complement and is stuck the function by the body 3.
2,Damage
It is specially sending lung fiber sign that upper skin cells are damaged. The virus infects and the inflammatory cell product (oxygen free-radical protein hydrolase) It is the intermediary material damaged. Upper leather cell damage, make plasma protein ooze out reach alveolus. In the course of damaging, the alveolus base ground floor can also be destroyed. Inflammatory cell (lymphocyte, macrophage, PMN) activated Existence make alveolus wall damage develop continuously.
3,Repair the fiber
Success to damage alveolus repair, demand, remove, enter the intersection of alveolus and plasma protein of, substitute the intersection of alveolus and wall that damage, store ground substance outside the cell that damage again. The alveolus formed while reacting in inflammation oozes out the liquid and includes a lot of cell factors, mediums such as growth factors (the intersection of blood platelet and growth factor, shift growth factor - the intersection of , and the intersection of insulin and kinds of growth factor - I) , the fiber connects plain, plain, fibrous peptide of thrombus,etc.. Skin cells and macrophages regulate cellulosic forming and clearance in the alveolus on the alveolus. Because of the existence of - PA, there is netted fibrin that degrades the activity in the alveolus. But person who send the intersection of lung and fiber take fibrin of patient in the BAL it degrades activities to be because fine to dissolve the intersection of zymogen and activator and fibrinolysin such as fine to dissolve zymogen activate inhibitor - 1 (PAI-1) specially Horizontal increased inhibitory. Likewise, the fibrous connection in the alveolus is plain but inhibited too. Oozing out liquid, removing, can become fibrous cell invade, hyperplasia in the alveolus, produce new the intersection of ground substance and albumen, make rich in cellulose to ooze out liquid to become cicatrix.
The intersection of peanut and four the intersection of alkene and until person who take place the intersection of lung and fiber that fiber take take react, playing an important role too specially sour supersession. Lie between and usually have a direct impact on quality while becoming fibrous cells and other cell in vain, stimulate into fibrous cells and release and trend towards the factor of melting, promote cell hyperplasia and collagen to formate. An important characteristic that the alveolus repairs is that the cover is re-formed on an alveolus basilar membrane. For finish course this, leather the intersection of cell and hyperplasia, final basilar membrane surface repair and part ooze out the liquid machine at the the intersection of Model 2 and alveolus. This course undoubtedly happens under angle cell growth factor and influence of hepatocyte growth factor, two factor these regulate upper leather hyperplasia of cell and move the conduct.
Specially in sending the lungs that the fibers take forming process,at lack cells leather,collapse alveolus, form the blocky cicatrix of group when involving a large number of alveoluses.
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