Editing Pulmonary alveolus (section)

====Structural====
[[File:Cryptococcosis of lung in patient with AIDS. Mucicarmine stain 962 lores.jpg|thumb|[[Cryptococcosis]] of lung in patient with AIDS. Mucicarmine stain. Histopathology of lung shows widened alveolar septum containing a few inflammatory cells and numerous yeasts of [[Cryptococcus neoformans]]. The inner layer of the yeast capsule stain red.]]

Almost any type of [[lung tumor]] or [[lung cancer]] can compress the alveoli and reduce gas exchange capacity. In some cases the tumor will fill the alveoli.<ref name="Spencer1">{{cite book | vauthors = Mooi W | chapter = Common Lung Cancers |title=Spencer's Pathology of the Lung.| veditors = Hasleton P |publisher=McGraw-Hill |year=1996 |isbn=0-07-105448-0 |location= New York |page=1076 |url= https://www.amazon.com/reader/0071054480}}</ref>
* [[Cavitary pneumonia]] is a process in which the alveoli are destroyed and produce a cavity. As the alveoli are destroyed, the surface area for gas exchange to occur becomes reduced. Further changes in blood flow can lead to decline in lung function.
* [[Emphysema]] is another disease of the lungs, whereby the [[elastin]] in the walls of the alveoli is broken down by an imbalance between the production of [[neutrophil elastase]] (elevated by cigarette smoke) and [[alpha-1 antitrypsin]] (the activity varies due to genetics or reaction of a critical methionine residue with toxins including cigarette smoke). The resulting loss of elasticity in the lungs leads to prolonged times for exhalation, which occurs through passive recoil of the expanded lung. This leads to a smaller volume of gas exchanged per breath.
* [[Pulmonary alveolar microlithiasis]] is a rare lung disorder of small stone formation in the alveoli.
* Several factors, including smoking, viral infections, and aging, contribute to physical damage to type II alveolar cells. Some studies have linked injury to these cells to the proliferation of [[fibrosis]] in the lungs and the onset of [[idiopathic pulmonary fibrosis]].<ref>{{Cite journal |last1=Parimon |first1=Tanyalak |last2=Yao |first2=Changfu |last3=Stripp |first3=Barry R |last4=Noble |first4=Paul W |last5=Chen |first5=Peter |date=2020-03-25 |title=Alveolar Epithelial Type II Cells as Drivers of Lung Fibrosis in Idiopathic Pulmonary Fibrosis |journal=International Journal of Molecular Sciences |language=en |volume=21 |issue=7 |pages=2269 |doi=10.3390/ijms21072269 |doi-access=free |issn=1422-0067 |pmc=7177323 |pmid=32218238}}</ref>