Pulmonary fibrosis animal models

Chemokines and Chemokine Receptors in Animal Models of Pulmonary Fibrosis... 

The mechanism finking chronic inflammation and tissue fibrosis is poorly understood. Various exposures and conditions are believed to cause pulmonary fibrosis. These include particulate agents, physical agents and infectious agents. To examine the pathogenesis of pulmonary fibrosis different experimental models in animals have been described. The most commonly used method to... 

Various studies have also examined animal models of pulmonary inflammation that are representative of primary eosinophil or neutrophil infiltration. Lung inflammation characterized by eosinophil influx has been used as a model of asthma and is not generally associated with lung fibrosis. After several episodes of repeated antigen challange, a subset of Ascaris -sensitive Cynomolgus monkeys developed a persistent eosinophilia and enhanced intercellular adhesion molecule-1 (ICAM-1) expression on pulmonary endothelial and epithelial cells when compared to control animals (Gundel etal., 1991, 1992). 

The possible functional role of decreased expression of IL-10 in pulmonary inflammation and bacterial clearance in cystic fibrosis has also been investigated in animal models. As might be surmised from the known properties of IL-10, these studies have collectively suggested that the reduced levels of IL-10 seen in adults with cystic fibrosis are associated with a potentiation of pulmonary inflammation and with an impairment of the clearance of P. aeruginosa. In a... 

Other animal models have been employed to more closely mimic IPF that can follow an acute lung injury. In this syndrome, the pulmonary fibrosis occurs as a result of a severe lung injury (acute lung injury/ARDS), resulting in severe complications, with secondary pulmonary hypertension and... 

Firfenidone is a novel agent that inhibits TGF-p in vitro and inhibits bleomycin-induced pulmonary fibrosis in animal models (202). Two uncontrolled, open-label... 

A host of other medications may lead to pulmonary complications. An exhaustive analysis of these medications is beyond the scope of this review. The adverse effect of supplemental oxygen is worth mentioning. Pulmonary toxicity is well established in animal models, but difficult to assess and quantify in patients treated for prolonged periods with high fraction of supplemental oxygen. Noncardiogenic pulmonary edema with DAD and secondary progression to pulmonary fibrosis are possible. 

Much of our current understanding of the pathogenesis of human lung fibrosis has come through the use of animal models. Of the various models studied, bleomycin-induced pulmonary fibrosis has received considerable attention. When administered intratracheally, intravenously, or intraperitoneally, bleomycin pro-... 

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