BIOM30001 Lecture Notes - Lecture 22: Goblet Cell, Chronic Obstructive Pulmonary Disease, Oxidative Stress
Document Summary
When stimulated by cigarette smoke--> epithelia/mphages release tgfb-->activates fibroblasts-->causes fibrosis of airways. Mphage release chemokines that attract t cells, neutrophils, monocytes. Proteases cause emphysema and mucus hypersecretion (goblet cell hyperplasia) --> bronchitis. Oxidative stress: cigarette smoke has oxidants that can destroy dna and interfere with mt function. May also play a role in glucocorticoid resistance in copd patients. Mphage and neutrophil play important role in clearing bac and maintaining lung health. Patients tend to have more bac in lower airways. Once cigarette smoke is removed, inflammation/reduced ability for mphage and nphil to clear bac/virus persists for many years. As disease progresses/symptoms increase, patients are more susceptible to viral and bac infections. May lead to hospitalization, decrease in quality of life - major cost of copd. Exacerbation due to infection/pollution -->more inflammation-->decrease in airway. Causes an increased need for or change in medication. Also associated with systemic inflammation leading to other comorbidities.
