Cystic fibrosis is a chronic, inherited, life threatening disease that affects organs in the body, because of sticky and thick mucus buildup on organs. The organs that are affected are the liver, lungs, pancreas, and intestine, which does damage to the respiratory, digestive and reproductive systems (Crosta). Cystic fibrosis is caused by a mutation in a gene called cystic fibrosis trans-membrane regulator, also called CFTR, which has an important function of creating sweat, mucus and digestive juices (Crostra). The CFTR gene is a transporter gene that contains codes that tells cells how to behave. It is also located in the seventh chromosome, in which it’s responsible for regulating salt and water movement between cells.
In asthmatic patient there would be hyperplasia and hypertrophy of airway smooth muscle stimulated by growth factors such as platelet-derived growth factors that are released from inflammatory cells. Basement membrane is also thickened due to subepithelial fibrosis with deposition of types III and V collagen. It occurs due to eosinophilic infiltration by release of profibrotic mediators such as transforming growth factor β. This fibrosis contributes to irreversible narrowing of airways. Inflammatory mediators may activate sensory nerves resulting in reflex cholinergic bronchoconstriction or release of inflammatory neuropeptides which further exacerbate asthma.
The mechanical pressures and stimulus cause changes to the extracellular matrix (ECM) as the processes of fibrogenesis and fibrolysis take place. The combined production and degradation of the ECM creates irregular fibrotic tissues. This can ultimately lead to greater difficulties in dealing with the condition as lung surface area is effectively being reduced. Further hyperresponsiveness behaviour of the smooth muscle cells will lead to further airway fibrosis (8,9). Fibrolysis is a process that involves the active enzyme plasminogen (10).
Retrieved from http://www.mayoclinic.org/diseases-conditions/pneumothorax/basics/definition/con-20030025?p=1 Schneider, F., Murali, R., Veraldi, K. L., Tazelaar, H. D., & Leslie, K. O. (2014). Approach to Lung Biopsies From Patients With Pneumothorax. Archives of Pathology & Laboratory Medicine, 138(2), 257-265. Uramoto, H., Shimokawa, H., & Tanaka, F. (2012).
During an asthma attack, the bronchial muscles tighten, the mucosa lining in the respiratory tract swell, and mucus production in respiratory tract excessively resulting in airway narrowing. The main origin factors of asthma are genetic predisposition to type I hypersensivity (atopy), acute and chronic airway inflammation, and bronchial hyperresponsiveness to a diversity of stimuli. The inflammation contains a lot of cell types and various inflammatory mediators, but the performance of type 2 helper T (TH2) cells may be demanding to the pathogenesis of asthma. The typical atopic form of asthma is related with an exorbitant TH2 reaction against environmental antigens. TH2 cells produce cytokines which is report for most of the properties of asthma—IgE (Immunoglobulin E) production stimulated by IL-4 (Interleukin 4), eosinophils activated by IL-5 (Interleukin 5), and IL-13 (Interleukin 13) stimulates mucus production and as well promotes IgE production by B cells.
Airway remodeling is a distinct characteristics of chronic asthma and has direct link to the severity of asthma (Lambrecht and Hammad 2012). Characterized by loss of epithelial integrity, enlargement of goblet cell and submucosal gland (Schroeder et al. 2012), thickening of basement membrane (Soltani et al. 2012), hypertrophy and hyperplasia of smooth muscle mass and fibrosis of subepithelial tissue (Berair et al. 2013), airway remodelling contributes to airway hyperresponsiveness and reversible obstruction in asthma.
SARS: Severe Acute Respiratory Syndrome Epidemics Series. New York: The Rosen Publishing Group. Severe acute respiratory syndrome (SARS). (2007, February 10). Retrieved May 5, 2014, from Infectious Diseases Epideomology and Surveillance: http://ideas.health.vic.gov.au/bluebook/sars.asp#mode Tang, K.-L., Lo, V. I., & Wong, C.-k. (2006).