Get ready to energize your life?
Top Offers Only Today
Support your health and step-up your mental focus
post in: News Date:24 Sep 2017, 14:37 views:1996
Current understanding of scented asthma defines it as an inflammatory disorder of the airways involving T cells, mast cells, and eosinophils. 1, while acute inflammation is a beneficial non-specific response silicon of tissues to injury that generally leads to repair and restoration of normal structure and function, asthma represents a chronic inflammatory process of the airways followed by healing, whose end result is characteristically an altered structure. The possibility that these structural changes might be implicated in at least some of the clinical manifestations of asthma has been investigated in depth only in the last 1015 years.
However, despite extensive research, a number smoke of important questions remain unanswered. The factors that initiate and perpetuate remodelling are incompletely understood.
It is not clear whether airway remodelling is a normal response to an abnormal injury or, alternatively, whether the remodelling/repair response is itself an abnormal response. In addition, while remodelling is generally believed to be disadvantageous, in some ways it may serve a protective function.
The balance between these effects in vivo is speculative. This review will outline the relevant morphological changes in the airway wall before discussing the possible consequences and reviewing what is known about the potential for pharmacotherapy to prevent or reverse these changes. What constitutes airway remodelling?
In addition to the inflammatory features mentioned earlier, the airway wall of patients with asthma is usually characterised by a number of structural changes that are grouped together under the umbrella term airway remodelling.
It is not known which one(s) are the most useful and relevant markers, although most work has been done on epithelial disruption, sub-basement membrane thickening, and smooth muscle hypertrophy (fig 1). These changes are structural although, in the broadest sense, airway remodelling encompasses both structural and functional consequences of altered airway morphology. Figure 1, comparison of (A) normal and (B, C) asthmatic airway wall showing epithelial damage, increased smooth muscle, inflammatory cell infiltration, and sub-basement membrane thickening.
The images in (A) and (B) have been stained with toluidine blue and the image in (C) has been stained with an antibody to collagen III. Epithelial damage, despite the variable preservation of airway epithelium in biopsy and necropsy specimens, careful sampling has revealed enhanced epithelial fragility and increased epithelial damage in asthma, 2 and the extent of this abnormality correlates with measures of airway reactivity.
3, this suggests that epithelial injury is not only a feature of asthma, but also appears to be related to asthma severity. Thickening of the lamina reticularis below the true basement membrane is a characteristic early feature of the asthmatic bronchus and has been termed subepithelial fibrosis or sub-basement membrane thickening. This thickening is associated with deposition of collagen I, collagen III, and fibronectin.