Editing Bronchiectasis (section)

==Pathophysiology==
[[File:Bronchiectasis Vicious Cycle Pathogenesis.png|thumb|"Vicious cycle" theory of the pathogenesis of bronchiectasis.]]
The development of bronchiectasis requires two factors: an initial injury to the lung (such as from infection, auto-immune destruction of lung tissue, or other destruction of lung tissue (as seen in [[gastroesophageal reflux disease]] or [[aspiration pneumonia|aspiration syndromes]])) which leads to impaired [[mucociliary clearance]], obstruction, or a defect in host defense.<ref name="O'Donnell NEJM" /><ref name="Mc2013" /> This triggers a host immune response from [[neutrophil]]s ([[Neutrophil elastase|elastases]]), [[reactive oxygen species]], and inflammatory [[cytokine]]s that results in progressive destruction of normal lung architecture. In particular, the [[elastic fiber]]s of [[bronchi]] are affected.<ref name="DAVIDSONS2010" /> The result is permanent abnormal dilation and destruction of the major bronchi and bronchiole walls.<ref name="Bronchiectasis">{{cite web |url= https://www.lecturio.com/concepts/bronchiectasis/ | title= Bronchiectasis | website= The Lecturio Medical Concept Library |access-date= 5 July 2021}}</ref>

Disordered neutrophil function is believed to play a role in the pathogenesis of bronchiectasis. [[Neutrophil extracellular traps]] (NETs), which are extracellular fibers secreted by neutrophils that are used to trap and destroy pathogens, are hyperactive in bronchiectasis. Increased NET activity is associated with more severe bronchiectasis.<ref name="O'Donnell NEJM" /> Neutrophil elastase, which is an extracellular protein secreted by neutrophils to destroy pathogens as well as host tissue, is also hyperactive in many cases of bronchiectasis.<ref name="O'Donnell NEJM" /> An increased neutrophil elastase activity is also associated with worse outcomes and more severe disease in bronchiectasis.<ref name="O'Donnell NEJM" /> The initial lung injury in bronchiectasis leads to an impaired mucociliary clearance of the lung airways, which leads to mucous stasis.<ref name="O'Donnell NEJM" /> This mucous stasis leads to bacterial colonization in bronchiectasis which leads to neutrophil activation.<ref name="O'Donnell NEJM" /> This neutrophil activation leads to further tissue destruction and airway distortion by neutrophils in addition to direct tissue destruction by the pathogenic bacteria.<ref name="O'Donnell NEJM" /> The distorted, damaged lung airways thus have impaired mucociliary clearance; leading to mucous stasis and bacterial colonization leading to further neutrophil activation and thus fueling a self-perpetuating "vicious cycle" of inflammation in bronchiectasis.<ref name="O'Donnell NEJM" /> This "vicious cycle" theory is the generally accepted explanation for the pathogenesis of bronchiectasis.<ref name=":02"/>

Endobronchial tuberculosis commonly leads to bronchiectasis, either from bronchial [[stenosis]] or secondary traction from fibrosis.<ref name=":6"/> Traction bronchiectasis characteristically affects peripheral bronchi (which lack [[cartilage]] support) in areas of end-stage fibrosis.<ref name=":7">{{EMedicine|article|354167|Bronchiectasis Imaging}}</ref>