Editing Pulmonary alveolus (section)

==Clinical significance==

===Diseases===
{{Main|Respiratory disease|Alveolar lung disease}}

====Surfactant====
Insufficient [[surfactant]] in the alveoli is one of the causes that can contribute to [[atelectasis]] (collapse of part or all of the lung). Without [[pulmonary surfactant]], atelectasis is a certainty.<ref>{{cite book | last = Saladin | first = Kenneth S. | name-list-style = vanc |title=Anatomy and Physiology: the unity of form and function | url = https://archive.org/details/isbn_9780073213736_4 | url-access = registration |publisher=McGraw Hill |location=New York |year=2007 |isbn=978-0-07-322804-4}}</ref> The severe condition of [[acute respiratory distress syndrome]] (ARDS) is caused by a deficiency or dysfunction of surfactant.<ref name="Sever">{{cite journal |vauthors=Sever N, Miličić G, Bodnar NO, Wu X, Rapoport TA |title=Mechanism of Lamellar Body Formation by Lung Surfactant Protein B |journal=Mol Cell |volume=81 |issue=1 |pages=49–66.e8 |date=January 2021 |pmid=33242393 |pmc=7797001 |doi=10.1016/j.molcel.2020.10.042 |url=}}</ref> Insufficient surfactant in the lungs of preterm infants causes [[infant respiratory distress syndrome]] (IRDS). The [[lecithin–sphingomyelin ratio]]  is a measure of fetal [[amniotic fluid]] to indicate lung maturity or immaturity.<ref name="AJP">{{cite journal |vauthors=St Clair C, Norwitz ER, Woensdregt K, Cackovic M, Shaw JA, Malkus H, Ehrenkranz RA, Illuzzi JL |title=The probability of neonatal respiratory distress syndrome as a function of gestational age and lecithin/sphingomyelin ratio |journal=Am J Perinatol |volume=25 |issue=8 |pages=473–80 |date=September 2008 |pmid=18773379 |pmc=3095020 |doi=10.1055/s-0028-1085066 |url=}}</ref> A low ratio indicates a risk factor for IRDS. [[Lecithin]] and [[sphingomyelin]] are two of the glycolipids of pulmonary surfactant.

Impaired surfactant regulation can cause an accumulation of surfactant proteins to build up in the alveoli in a condition called [[pulmonary alveolar proteinosis]]. This results in impaired gas exchange.<ref name="Kumar">{{cite journal |last1=Kumar |first1=A |last2=Abdelmalak |first2=B |last3=Inoue |first3=Y |last4=Culver |first4=DA |title=Pulmonary alveolar proteinosis in adults: pathophysiology and clinical approach. |journal=The Lancet. Respiratory Medicine |date=July 2018 |volume=6 |issue=7 |pages=554–565 |doi=10.1016/S2213-2600(18)30043-2 |pmid=29397349|s2cid=27932336}}</ref>

====Inflammation====
[[Pneumonia]] is an [[inflammation|inflammatory condition]] of the [[Lung parenchyma|lung tissue]], which can be caused by both [[virus]]es and [[bacteria]]. [[Cytokine]]s and fluids are released into the alveolar cavity, [[pulmonary interstitium|interstitium]], or both, in response to infection, causing the effective surface area of gas exchange to be reduced. In severe cases where [[cellular respiration]] cannot be maintained, [[supplemental oxygen]] may be required.<ref>{{cite web |url= https://www.mayoclinic.org/diseases-conditions/pneumonia/symptoms-causes/syc-20354204 |title=Pneumonia – Symptoms and causes| work =Mayo Clinic |language=en|access-date=2019-06-10}}</ref><ref>{{Cite web|url=https://www.lung.org/lung-health-and-diseases/lung-disease-lookup/pneumonia/symptoms-and-diagnosis.html|title=Pneumonia Symptoms and Diagnosis|website=American Lung Association|language=en|access-date=2019-06-10}}</ref>
* [[Diffuse alveolar damage]] can be a cause of [[acute respiratory distress syndrome]](ARDS) a severe inflammatory disease of the lung.<ref name="DAVIDSONS2010">{{cite book | first1 = Nicki R | last1 = Colledge | first2 = Brian R | last2 = Walker | first3 = Stuart | last3 = Ralston | first4 = Stanley | last4 = Davidson | name-list-style = vanc |title=Davidson's principles and practice of medicine.|date=2010|publisher=Churchill Livingstone/Elsevier|location=Edinburgh|isbn=978-0-7020-3085-7|edition=21st}}</ref>{{rp|187}}
* In [[asthma]], the [[bronchiole]]s become narrowed, causing the amount of air flow into the lung tissue to be greatly reduced. It can be triggered by irritants in the air, [[photochemical smog]] for example, as well as substances to which a person is allergic.
* [[Bronchitis#Chronic bronchitis|Chronic bronchitis]] occurs when an [[Mucus hypersecretion|abundance of mucus]] is produced by the lungs. The production of mucus occurs naturally when the lung tissue is exposed to irritants. In chronic bronchitis, the air passages into the alveoli, the respiratory bronchioles, become clogged with mucus. This causes increased coughing in order to remove the mucus, and is often a result of extended periods of exposure to cigarette smoke.
* [[Hypersensitivity pneumonitis]]

====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>

====Fluid====
A [[pulmonary contusion]] is a [[bruise]] of the lung tissue caused by trauma.<ref>{{Cite web|url=https://www.merckmanuals.com/home/injuries-and-poisoning/chest-injuries/pulmonary-contusion|title=Pulmonary Contusion – Injuries and Poisoning|website=Merck Manuals Consumer Version|language=en-US|access-date=2019-06-10}}</ref> Damaged capillaries from a contusion can cause blood and other fluids to accumulate in the tissue of the lung, impairing gas exchange.

[[Pulmonary edema]] is the buildup of fluid in the parenchyma and alveoli. An edema is usually caused by left ventricular heart failure, or by damage to the lung or its vasculature.

==== Coronavirus ====
{{Further|ACE2#Coronavirus entry point}}
Because of the high expression of [[angiotensin-converting enzyme 2]] (ACE2) in type II alveolar cells, the lungs are susceptible to infections by some [[coronavirus]]es including the [[RNA virus|viruses]] that cause [[severe acute respiratory syndrome]] (SARS)<ref name="pmid20599443">{{cite journal | vauthors = Kuba K, Imai Y, Ohto-Nakanishi T, Penninger JM | title = Trilogy of ACE2: a peptidase in the renin-angiotensin system, a SARS receptor, and a partner for amino acid transporters | journal = Pharmacology & Therapeutics | volume = 128 | issue = 1 | pages = 119–28 | date = October 2010 | pmid = 20599443 | pmc = 7112678 | doi = 10.1016/j.pharmthera.2010.06.003}}</ref> and [[coronavirus disease 2019]] (COVID-19).<ref name="pmid32094336">{{cite journal | vauthors = Xu H, Zhong L, Deng J, Peng J, Dan H, Zeng X, Li T, Chen Q | display-authors = 6 | title = High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa | journal = International Journal of Oral Science | volume = 12 | issue = 1 | page = 8 | date = February 2020 | pmid = 32094336 | pmc = 7039956 | doi = 10.1038/s41368-020-0074-x}}</ref>