Bronchial inflammation eosinophils role

Although complementary mechanisms may exist, it is apparent that the accumulation of eosinophils is an important event in the development of chronic bronchial inflammation and asthma. While IL-5 is undoubtedly a key cytokine in this process, others such as IL-3 and GM-CSF may also play a role (Humbert,... 

Asthma has been traditionally viewed as a chronic inflammatory condition characterized by airway infiltration by activated mast cells and eosinophils, orchestrated by specific Th2-type T lymphocytes (24). However, neutrophils have recently been implicated in more severe forms of asthma, and it is also increasingly evident that the bronchial epithelium, endothelium, fibroblasts, and the extracellular matrix play a dynamic role in the airway inflammation of asthma (Fig. 2). 

Bronchial biopsies in stable atopic asthmatics have observed these components (19,64). Several Th2-type cytokines, (IL-4, IL-5, IL-13, but not JFNy) and C-C chemokines are produced by multiple cells types, which regulate IgE synthesis and lead to the generation of eosinophilic airway inflammation (Fig. 9) (321). Allergic tissue damage results from the release of basic proteins, leukotrienes, and PAF secreted by activated eosinophils. It is clear that the mast cell plays an important role in the immediate response and that T cells play a key role in orchestrating the nature and severity of the inflammation by the secretion of cytokines. As stated earlier, the eosinophil is regarded as the primary effector cell due to the capacity to secrete major basic protein and eosinophil cationic protein, which have profound cytotoxic effects on the airway epithelium (316). 

Over a decade of research and clinical efforts in the immunopathogenesis of asthma (1,2) have substantiated the critical role of airway inflammation and identified key mediators and mechanisms. Because information on the pathological features of asthma was first obtained from postmortem examination of severe asthmatics, airway inflammation was believed to be a feature of advanced, terminal disease (3). Those airways showed infiltration by granulocytes (neutrophils, eosinophils), increased numbers of lymphocytes, activated mast cells, collagen deposition beneath the basement membrane, and occlusion of the bronchial lumen by mucus produced from hyperplastic goblet cells. The finding of hypertrophied bronchial smooth muscle supported the widely held belief that asthma was primarily a disease of airway smooth muscle. 

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