Editing Pulmonary alveolus

{{short description|Hollow cavity found in the lungs}}
{{use dmy dates|date=December 2024}}
{{other uses|Alveolus (disambiguation){{!}}Alveolus}}
{{Infobox anatomy
| Name      = Pulmonary alveolus
| Latin     = alveolus pulmonis
| Image     = Alveolus diagram.svg
| Caption   = The alveoli
| Image2    = 
| Caption2  = 
| Precursor = 
| System    = [[Respiratory system]] 
| Location  = [[Lung]]
| Artery    = 
| Vein      = 
| Nerve     = 
| Lymph     = 
}}

A '''pulmonary alveolus''' ({{plural abbr|'''alveoli'''}}; {{etymology|la|{{wikt-lang|la|alveolus}}|little cavity}}), also called an '''air sac''' or '''air space''', is one of millions of hollow, distensible cup-shaped cavities in the [[lung]]s where pulmonary gas exchange takes place.<ref name="MeSH1">{{cite web |title=Pulmonary Gas Exchange - MeSH |publisher=[[National Center for Biotechnology Information|NCBI]] |url=https://ncbi.nlm.nih.gov/mesh/?term=pulmonary+gas+exchange |website=ncbi.nlm.nih.gov |access-date=2022-12-30}}</ref> [[Oxygen]] is [[Molecular diffusion#Biology|exchanged]] for [[carbon dioxide]] at the [[blood–air barrier]] between the alveolar air and the [[Pulmonary circulation|pulmonary capillary]].<ref name="SEER">{{cite web |title=Alveoli |url=https://cancer.gov/publications/dictionaries/cancer-terms/def/alveoli |publisher=[[National Cancer Institute]] |website=cancer.gov |language=en |date=2011-02-02 |access-date=2021-07-22}}</ref> Alveoli make up the functional tissue of the [[mammal]]ian lungs known as the [[lung parenchyma]], which takes up 90 percent of the total lung volume.<ref name="Knudsen"/><ref name="Jones">{{cite web |last=Jones|first=Jeremy |title=Lung parenchyma {{!}} Radiology Reference Article |url=https://radiopaedia.org/articles/lung-parenchyma?lang=gb |publisher=[[Radiopaedia]] |access-date=2021-08-15}}</ref>

Alveoli are first located in the [[respiratory bronchiole]]s that mark the beginning of the  [[respiratory zone]]. They are located sparsely in these bronchioles, line the walls of the [[alveolar duct]]s, and are more numerous in the blind-ended [[alveolar sac]]s.<ref name="Moore"/> The [[Pulmonary acinus|acini]] are the basic units of respiration, with [[gas exchange]] taking place in all the alveoli present.<ref>{{cite journal | vauthors = Hansen JE, Ampaya EP, Bryant GH, Navin JJ | title = Branching pattern of airways and air spaces of a single human terminal bronchiole | journal = Journal of Applied Physiology | volume = 38 | issue = 6 | pages = 983–9 | date = June 1975 | pmid = 1141138 | doi = 10.1152/jappl.1975.38.6.983}}</ref> The alveolar membrane is the gas exchange surface, surrounded by a network of [[capillary|capillaries]]. Oxygen is [[Diffusion#Diffusion vs. bulk flow|diffused]] across the membrane into the capillaries and carbon dioxide is released from the capillaries into the alveoli to be breathed out.<ref>{{cite encyclopedia | vauthors = Hogan CM | veditors = McGinley M, Cleveland CJ | date = 2011 | chapter-url = https://editors.eol.org/eoearth/wiki/Respiration | chapter = Respiration | title = Encyclopedia of Earth | publisher = National council for Science and the Environment. | location = Washington, D.C.}}</ref><ref>{{cite book | first1 = Steve | last1 = Paxton | first2 = Michelle| last2 = Peckham| first3 = Adele | last3 = Knibbs | name-list-style = vanc |section=Functions of the Respiratory Portion |title=The Leeds Histology Guide | publisher = Faculty of Biological Sciences, University of Leeds |section-url=http://www.histology.leeds.ac.uk/respiratory/respiratory.php |date=2003}}</ref>

Alveoli are particular to mammalian lungs. Different structures are involved in gas exchange in other vertebrates.<ref>{{cite journal | vauthors = Daniels CB, Orgeig S | title = Pulmonary surfactant: the key to the evolution of air breathing | journal = News in Physiological Sciences | volume = 18 | issue = 4 | pages = 151–7 | date = August 2003 | pmid = 12869615 | doi = 10.1152/nips.01438.2003}}</ref>

== Structure ==
[[File:Bronchial anatomy with description.png|thumb|upright=1.4|[[Bronchiole|Bronchial]] anatomy showing [[terminal bronchioles]] (BT) leading to [[respiratory bronchiole]]s (BR) and alveolar ducts (DA) that open into alveolar sacs containing out pockets of alveoli (A) separated by [[alveolar septum|alveolar septa]] (AS)]]
The alveoli are first located in the respiratory bronchioles as scattered outpockets, extending from their lumens. The respiratory bronchioles run for considerable lengths and become increasingly alveolated with side branches of '''alveolar ducts''' that become deeply lined with alveoli. The ducts number between two and eleven from each bronchiole.<ref name="Spencer 2">{{cite book |title=Spencer's pathology of the lung |date=1996 |publisher=McGraw-Hill |location=New York |isbn=0-07-105448-0 |pages=22–25 |edition=5th}}</ref> Each duct opens into five or six '''alveolar sacs''' into which clusters of alveoli open.

Each terminal respiratory unit is called an [[Lung#Respiratory zone|acinus]] and consists of the respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli. New alveoli continue to form until the age of eight years.<ref name="Moore">{{cite book |title=Clinically oriented anatomy |last=Moore|first=Keith | name-list-style = vanc |publisher=Wolters Kluwer |year=2018 |isbn=978-1-4963-4721-3 |page=336}}</ref>

A typical pair of [[Lung|human lungs]] contains about 480 million alveoli,<ref name="pmid14512270">{{cite journal | vauthors = Ochs M | title = The number of alveoli in the human lung | journal = Am J Respir Crit Care Med | volume = 1 | issue = 169 | pages = 120–4 | date = 2004 | pmid = 14512270 | doi = 10.1164/rccm.200308-1107OC}}</ref> providing a total surface area for gas exchange of between 70 and 80 square metres.<ref name="Spencer 2"/> Each alveolus is wrapped in a fine mesh of [[capillaries]] covering about 70% of its area.<ref name="Saladin"/> The diameter of an alveolus is between 200 and 500 [[micrometre|μm]].<ref name="Saladin">Stanton, Bruce M.; Koeppen, Bruce A., eds. (2008). Berne & Levy physiology (6th ed.). Philadelphia: Mosby/Elsevier. pp. 418–422. {{ISBN|978-0-323-04582-7}}.</ref>

=== Microanatomy ===
An alveolus consists of an [[epithelial]] layer of simple [[Epithelium#Cell types|squamous epithelium]] (very thin, flattened cells),<ref name=NIH>{{cite web |url= https://training.seer.cancer.gov/anatomy/respiratory/passages/bronchi.html |title=Bronchi, Bronchial Tree & Lungs | work = SEER Training Modules | publisher = U.S. Department of Health and Human Services National Institutes of Health National Cancer Institute}}</ref> and an [[extracellular matrix]] surrounded by [[Capillary|capillaries]]. The epithelial lining is part of the alveolar membrane, also known as the respiratory membrane, that allows the [[gas exchange|exchange of gases]]. The membrane has several layers – a layer of [[alveolar lining fluid]] that contains [[surfactant]], the epithelial layer and its basement membrane; a thin [[interstitium|interstitial space]] between the epithelial lining and the capillary membrane; a capillary basement membrane that often fuses with the alveolar basement membrane, and the capillary [[endothelial]] membrane. The whole membrane however is only between 0.2 [[micrometre|μm]] at its thinnest part and 0.6 μm at its thickest.<ref name="Hall">{{Cite book|title=Guyton and Hall Textbook of Medical Physiology|last=Hall|first=John | name-list-style = vanc |publisher=Saunders Elsevier|year=2011|isbn=978-1-4160-4574-8|pages=489–491}}</ref>

In the '''alveolar walls''' there are interconnecting air passages between the alveoli known as the [[pores of Kohn]]. The '''alveolar septum''' that separates the alveoli in the alveolar sac contains some [[collagen |collagen fibers]] and [[elastic fibers]]. The septa also house the enmeshed capillary network that surrounds each alveolus.<ref name="Knudsen"/> The elastic fibres allow the alveoli to stretch when they fill with air during inhalation. They then spring back during exhalation in order to expel the carbon dioxide-rich air.
[[File:Alveolar sac.JPG|thumb|A histologic slide of a human alveolar sac]]

There are three major types of '''alveolar cell'''. Two types are '''pneumocytes''' or '''pneumonocytes''' known as type I and type II cells found in the alveolar wall, and a large [[phagocyte|phagocytic cell]] known as an [[alveolar macrophage]] that moves about in the lumens of the alveoli, and in the connective tissue between them. Type I cells, also called type I pneumocytes, or type I alveolar cells, are squamous, thin and flat and form the structure of the alveoli. Type II cells, also called type II pneumocytes or type II alveolar cells, release [[pulmonary surfactant]] to lower [[surface tension]], and can also [[cellular differentiation|differentiate]] to replace damaged type I cells.<ref name="Saladin"/><ref name="Naeem">{{cite journal |last1=Naeem |first1=Ahmed |last2=Rai |first2=Sachchida N. |last3=Pierre |first3=Louisdon |title=Histology, Alveolar Macrophages |url=https://www.ncbi.nlm.nih.gov/books/NBK513313/ |website=StatPearls |publisher=StatPearls Publishing |access-date=12 September 2021 |date=2021|pmid=30020685}}</ref>

== Development ==
Development of the earliest structures that will contain alveoli begins on day 22 and is divided into five stages: embryonic, pseudoglandular, canalicular, saccular, and alveolar stage.<ref name="Embryology, Pulmonary">{{cite book | vauthors = Rehman S, Bacha D | title = Embryology, Pulmonary |publisher=StatPearls Publishing|date = August 8, 2022| pmid = 31335092}}</ref> The alveolar stage begins approximately 36 weeks into development. Immature alveoli appear as bulges from the sacculi which invade the primary septa. As the sacculi develop, the protrusions in the primary septa become larger; new septations are longer and thinner and are known as secondary septa.<ref name="Embryology, Pulmonary" /> Secondary septa are responsible for the final division of the sacculi into alveoli. Majority of alveolar division occurs within the first 6 months but continue to develop until 3 years of age. To create a thinner diffusion barrier, the double-layer capillary network fuse into one network, each one closely associated with two alveoli as they develop.<ref name="Embryology, Pulmonary" />

In the first three years of life, the enlargement of lungs is a consequence of the increasing number of alveoli; after this point, both the number and size of alveoli increases until the development of lungs finishes at approximately 8 years of age.<ref name="Embryology, Pulmonary" />

== Function ==
[[File:An annotated diagram of an alveolus.svg|thumb|An annotated diagram of the alveolus]]

===Type I cells===
[[File:Cross section of an alveolus and capillaries showing diffusion of gases.svg|thumb|The cross section of an alveolus with capillaries is shown. Part of the cross section is magnified to show diffusion of oxygen gas and carbon dioxide through type I cells and capillary cells.]]
[[File:Gas exchange in the aveolus.svg|thumb|Gas exchange in the alveolus]]
Type I cells are the larger of the two cell types; they are thin, flat epithelial lining cells (membranous pneumocytes), that form the structure of the alveoli.<ref name="Knudsen">{{cite journal |last1=Knudsen |first1=L |last2=Ochs |first2=M |title=The micromechanics of lung alveoli: structure and function of surfactant and tissue components. |journal=Histochemistry and Cell Biology |date=December 2018 |volume=150 |issue=6 |pages=661–676 |doi=10.1007/s00418-018-1747-9 |pmid=30390118|pmc=6267411}}</ref> They are squamous (giving more surface area to each cell) and have long cytoplasmic extensions that cover more than 95% of the alveolar surface.<ref name="Saladin"/><ref name="Weinberger">{{cite book |last1=Weinberger |first1=Steven |last2=Cockrill |first2=Barbara |last3=Mandell |first3=Jess | name-list-style = vanc |title=Principles of pulmonary medicine |date=2019 |publisher=Elsevier |isbn=978-0-323-52371-4 |pages=126–129 |edition=Seventh}}</ref>

Type I cells are involved in the process of [[gas exchange]] between the alveoli and [[blood]]. These cells are extremely thin – sometimes only 25&nbsp;nm – the [[electron microscope]] was needed to prove that all alveoli are lined with [[epithelium]]. This thin lining enables a fast [[Diffusion#Diffusion vs. bulk flow|diffusion]] of [[gas exchange]] between the air in the alveoli and the [[blood]] in the surrounding capillaries.

The nucleus of a type I cell occupies a large area of free cytoplasm and its [[organelle]]s are clustered around it reducing the thickness of the cell. This also keeps the thickness of the [[blood-air barrier]] reduced to a minimum.

The cytoplasm in the thin portion contains [[Pinocytosis|pinocytotic vesicles]] which may play a role in the removal of small particulate contaminants from the outer surface. In addition to [[desmosome]]s, all type I alveolar cells have occluding junctions that prevent the leakage of tissue fluid into the alveolar air space.

The relatively low solubility (and hence rate of diffusion) of oxygen necessitates the large internal surface area (about 80 square m [96 square yards]) and very thin walls of the alveoli. Weaving between the capillaries and helping to support them is an [[extracellular matrix]], a meshlike fabric of elastic and collagenous fibres. The collagen fibres, being more rigid, give the wall firmness, while the elastic fibres permit expansion and contraction of the walls during breathing.

Type I pneumocytes are unable to [[mitosis|replicate]] and are susceptible to toxic [[Insult (medical)|insults]]. In the event of damage, type II cells can proliferate and differentiate into type I cells to compensate.<ref name=":0" />

===Type II cells===
Type II cells are cuboidal and much smaller than type I cells.<ref name="Knudsen"/> They are the most numerous cells in the alveoli, yet do not cover as much surface area as the squamous type I cells.<ref name=":0">{{Cite book |title=Gray's Anatomy: the anatomical basis of clinical practice |date=2021 |publisher=Elsevier |isbn=978-0-7020-7705-0 |editor-last=Gray |editor-first=Henry |edition=42nd |location=Amsterdam |pages=1035 |editor-last2=Standring |editor-first2=Susan |editor-last3=Anhand |editor-first3=Neel}}</ref> Type II cells (granulous pneumocytes) in the alveolar wall contain secretory [[organelle]]s known as [[lamellar bodies]] or lamellar granules, that fuse with the cell membranes and secrete [[pulmonary surfactant]]. This surfactant is a film of fatty substances, a group of [[phospholipid]]s that reduce alveolar [[surface tension]]. The phospholipids are stored in the lamellar bodies. Without this coating, the alveoli would collapse. The surfactant is continuously released by [[exocytosis]]. Reinflation of the alveoli following exhalation is made easier by the surfactant, which reduces surface tension in the thin [[Epithelial lining fluid|fluid lining of the alveoli]]. The fluid coating is produced by the body in order to facilitate the transfer of gases between blood and alveolar air, and the type II cells are typically found at the [[blood–air barrier]].<ref>{{cite book | title = Histology, A Text and Atlas | edition = Sixth | date = 2011 | last1 = Ross | first1 = Michael H | last2 = Pawlina | first2 = Wojciech | name-list-style = vanc}}</ref><ref name="pmid11686863">{{cite journal | vauthors = Fehrenbach H | title = Alveolar epithelial type II cell: defender of the alveolus revisited | journal = Respiratory Research | volume = 2 | issue = 1 | pages = 33–46 | date = 2001 | pmid = 11686863 | pmc = 59567 | doi = 10.1186/rr36 | doi-access = free}}</ref>

Type II cells start to develop at about 26 weeks of [[gestation]], secreting small amounts of surfactant. However, adequate amounts of surfactant are not secreted until about 35 weeks of gestation – this is the main reason for increased rates of [[infant respiratory distress syndrome]], which drastically reduces at ages above 35 weeks gestation.

Type II cells are also capable of cellular division, giving rise to more type I and II alveolar cells when the lung tissue is damaged.<ref>{{cite web|url=https://ntp.niehs.nih.gov/nnl/respiratory/lung/regen/index.htm|title=Lung – Regeneration – Nonneoplastic Lesion Atlas| work = National Toxicology Program | publisher =  National Institute of Environmental Health Sciences, National Institutes of Health, U.S. Department of Health and Human Services |access-date=2018-05-18}}</ref>

''[[MUC1]]'', a human [[gene]] associated with type II pneumocytes, has been identified as a marker in [[lung cancer]].<ref name="pmid9850098">{{cite journal | vauthors = Jarrard JA, Linnoila RI, Lee H, Steinberg SM, Witschi H, Szabo E | title = MUC1 is a novel marker for the type II pneumocyte lineage during lung carcinogenesis | journal = Cancer Research | volume = 58 | issue = 23 | pages = 5582–9 | date = December 1998 | pmid = 9850098 | url = http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&pmid=9850098}}</ref>

The importance of the type 2 lung alveolar cells in the development of severe respiratory symptoms of COVID-19 and potential mechanisms on how these cells are protected by the SSRIs fluvoxamine and fluoxetine was summarized in a review in April 2022.<ref>{{Cite journal |last1=Mahdi |first1=Mohamed |last2=Hermán |first2=Levente |last3=Réthelyi |first3=János M. |last4=Bálint |first4=Bálint László |date=January 2022 |title=Potential Role of the Antidepressants Fluoxetine and Fluvoxamine in the Treatment of COVID-19 |journal=International Journal of Molecular Sciences |language=en |volume=23 |issue=7 |page=3812 |doi=10.3390/ijms23073812 | pmid=35409171 |pmc=8998734 |issn=1422-0067|doi-access=free}}</ref>

===Alveolar macrophages===
The [[alveolar macrophage]]s reside on the internal luminal surfaces of the alveoli, the alveolar ducts, and the bronchioles. They are mobile scavengers that serve to engulf foreign particles in the lungs, such as dust, bacteria, carbon particles, and blood cells from injuries.<ref>{{cite encyclopedia | chapter = The trachea and the stem bronchi | chapter-url = http://www.britannica.com/EBchecked/topic/483141/pulmonary-alveolus | title = Encyclopædia Britannica | publisher = Encyclopædia Britannica, Inc.}}</ref> They are also called ''pulmonary macrophages'', and ''dust cells''. Alveolar macrophages also play a crucial role in immune responses against viral pathogens in the lungs.<ref name=":1">{{Cite journal |last1=Malainou |first1=Christina |last2=Abdin |first2=Shifaa M. |last3=Lachmann |first3=Nico |last4=Matt |first4=Ulrich |last5=Herold |first5=Susanne |date=2023-10-02 |title=Alveolar macrophages in tissue homeostasis, inflammation, and infection: evolving concepts of therapeutic targeting |url=https://www.jci.org/articles/view/170501 |journal=Journal of Clinical Investigation |language=en |volume=133 |issue=19 |doi=10.1172/JCI170501 |issn=1558-8238 |pmc=10541196 |pmid=37781922}}</ref> They secrete cytokines and chemokines, which recruit and activate other immune cells, initiate type I interferon signaling, and inhibit the nuclear export of viral genomes.<ref name=":1" /> 

==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>

==Additional images==
<gallery>
File:Pulmonary Blood Circulation.png|Blood circulation around alveoli
File:Plain home talk about the human system-the habits of men and women-the cause and prevention of disease-our sexual relations and social natures (1896) (14577681128).jpg|Diagrammatic view of lung showing magnified inner structures including alveolar sacs at 10) and lobules at 9)
</gallery>

== See also ==
* [[Interstitial lung disease]]
* [[A549 cell]]s
* [[List of distinct cell types in the adult human body]]

== References ==
{{Reflist}}

== External links ==
{{Commons category}}
* {{MeSH name|Pulmonary+Alveoli}}

{{Lung}}
{{Authority control}}

{{DEFAULTSORT:Pulmonary Alveolus}}
[[Category:Lung anatomy]]
[[Category:Respiratory system anatomy]]