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{{Short description|Category of white blood cells}}
{{Infobox cell
| Name = Granulocyte
| Image = Types of granulocytes.png
| Caption = Types of granulocytes
| Width = 320
| System = [[Immune system]]
}}

'''Granulocytes''' are cells in the [[innate immune system]] characterized by the presence of [[specific granule]]s in their [[cytoplasm]].<ref>{{cite book |author=WebMD |chapter=granulocyte |chapter-url=https://books.google.com/books?id=t8UfI3BH78wC&pg=PA181 |page=181 |year=2009 |title=Webster's New World Medical Dictionary |edition=3rd |publisher=Houghton Mifflin Harcourt |isbn=978-0-544-18897-6}}</ref> Such granules distinguish them from the various [[agranulocyte]]s. All [[myeloblast]]ic granulocytes are polymorphonuclear, that is, they have varying shapes (morphology) of the [[cell nucleus|nucleus]] (segmented, irregular; often lobed into three segments); and are referred to as '''polymorphonuclear leukocytes''' ('''PMN''', '''PML''', or '''PMNL'''). In common terms, ''polymorphonuclear granulocyte'' refers specifically to "[[neutrophil]] granulocytes",<ref>{{cite book |author=WebMD |chapter=leukocyte, polymorphonuclear |chapter-url=https://books.google.com/books?id=t8UfI3BH78wC&pg=PA244 |page=244 |year=2009 |title=Webster's New World Medical Dictionary |edition=3rd |publisher=Houghton Mifflin Harcourt |isbn=978-0-544-18897-6}}</ref> the most abundant of the granulocytes; the other types ([[eosinophil]]s, [[basophil]]s, and [[mast cell]]s) have varying morphology. Granulocytes are produced via [[granulopoiesis]] in the [[bone marrow]].

==Types==
[[Image:1907 Granular Leukocytes.jpg|thumb|Granulocytes with names derived from their [[staining (biology)|staining]] characteristics]]
There are four types of granulocytes (full name polymorphonuclear granulocytes):<ref name="Granulocyte 2017 review">{{cite journal | vauthors = Breedveld A, Groot Kormelink T, van Egmond M, de Jong EC | title = Granulocytes as modulators of dendritic cell function | journal = Journal of Leukocyte Biology | volume = 102 | issue = 4 | pages = 1003–16 | date = October 2017 | pmid = 28642280 | doi = 10.1189/jlb.4MR0217-048RR | doi-access = free }}</ref>
* [[Basophil]]s
* [[Eosinophil]]s
* [[Neutrophil]]s
* [[Mast cell]]s

Except for the mast cells, their names are derived from their [[staining (biology)|staining]] characteristics; for example, the most abundant granulocyte is the [[neutrophil granulocyte]], which has neutrally staining [[cytoplasm]]ic granules.<ref>{{cite journal |vauthors=Wittekind D |title=On the nature of Romanowsky dyes and the Romanowsky-Giemsa effect |journal=Clin Lab Haematol |volume=1 |issue=4 |pages=247–62 |date=1979 |pmid=94558 |doi=10.1111/j.1365-2257.1979.tb01090.x }}</ref>

===Neutrophils===
{{main|Neutrophil}}
[[Image:Neutrophil2.jpg|thumb|A neutrophil with a segmented nucleus (center and surrounded by [[erythrocytes]]), the intra-cellular granules are visible in the [[cytoplasm]] ([[Giemsa stain|Giemsa-stained]] high magnification)]]
Neutrophils are normally found in the [[circulatory system|bloodstream]] and are the most abundant type of [[phagocyte]], constituting 60% to 65% of the total circulating white blood cells,<ref name="IandF">{{cite book | last = Stvrtinová | first = Viera | author2 = Ján Jakubovský and Ivan Hulín | title = Inflammation and Fever from Pathophysiology: Principles of Disease | publisher = Academic Electronic Press | year = 1995 | location = Computing Centre, Slovak Academy of Sciences | url = http://nic.sav.sk/logos/books/scientific/node15.html | isbn = 80-967366-1-2 | access-date = March 28, 2009 | chapter = Neutrophils, central cells in acute inflammation | archive-url = https://web.archive.org/web/20101231014453/http://nic.sav.sk/logos/books/scientific/node15.html | archive-date = December 31, 2010 }}</ref> and consisting of two [[Neutrophil#Subpopulations|subpopulations]]: neutrophil-killers and neutrophil-cagers. One litre of human blood contains about five billion neutrophils,<ref name=Hoff-values>{{harvnb|Hoffbrand|Pettit|Moss|2005|p=331}}</ref> which are about 12–15 [[micrometre]]s in diameter.<ref name=autogenerated2>Abbas, Chapter 12, 5th Edition{{full citation needed|date=May 2015}}{{page needed|date=May 2015}} </ref> Once neutrophils have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection.<ref name=Som18>{{harvnb|Sompayrac|2008|p=18}}</ref> Neutrophils do not return to the blood; they turn into [[pus]] cells and die.<ref name=Som18/> Mature neutrophils are smaller than monocytes, and have a segmented [[Cell nucleus|nucleus]] with several sections(two to five segments); each section is connected by [[chromatin]] filaments. Neutrophils do not normally exit the bone marrow until maturity, but during an infection neutrophil precursors called [[myelocyte]]s and [[promyelocyte]]s are released.<ref name="pmid9853933">{{cite journal | vauthors = Linderkamp O, Ruef P, Brenner B, Gulbins E, Lang F | title = Passive deformability of mature, immature, and active neutrophils in healthy and septicemic neonates | journal = Pediatric Research | volume = 44 | issue = 6 | pages = 946–50 | date = December 1998 | pmid = 9853933 | doi = 10.1203/00006450-199812000-00021 | doi-access = free }}</ref>

Neutrophils have three strategies for directly attacking micro-organisms: [[phagocytosis]] (ingestion), release of soluble anti-microbials (including granule proteins), and generation of [[neutrophil extracellular traps]] (NETs).<ref name="NatRev">{{cite journal | vauthors = Hickey MJ, Kubes P | title = Intravascular immunity: the host-pathogen encounter in blood vessels | journal = Nature Reviews. Immunology | volume = 9 | issue = 5 | pages = 364–75 | date = May 2009 | pmid = 19390567 | doi = 10.1038/nri2532 | s2cid = 8068543 }}</ref>
Neutrophils are professional [[phagocytes]]:<ref name= Rob>{{harvnb|Robinson|Babcock|1998|p=187}}<br/>{{harvnb|Ernst|Stendahl|2006|pp=7–10}}</ref> they are ferocious eaters and rapidly engulf invaders coated with [[antibody|antibodies]] and [[complement system|complement]], as well as damaged cells or cellular debris. The intracellular granules of the human neutrophil have long been recognized for their protein-destroying and bactericidal properties.<ref>{{harvnb|Paoletti|Notario|Ricevuti|1997|p=62}}</ref> Neutrophils can secrete products that stimulate monocytes and [[macrophage]]s; these secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing.<ref name="pmid17991288">{{cite journal | vauthors = Soehnlein O, Kenne E, Rotzius P, Eriksson EE, Lindbom L | title = Neutrophil secretion products regulate anti-bacterial activity in monocytes and macrophages | journal = Clinical and Experimental Immunology | volume = 151 | issue = 1 | pages = 139–45 | date = January 2008 | pmid = 17991288 | pmc = 2276935 | doi = 10.1111/j.1365-2249.2007.03532.x }}</ref>

Neutrophils have two types of granules; primary (azurophilic) granules (found in young cells) and [[specific granules|secondary (specific) granules]] (which are found in more mature cells). Primary granules contain cationic proteins and [[defensin]]s that are used to kill bacteria, proteolytic enzymes and cathepsin G to break down (bacterial) proteins, lysozyme to break down bacterial [[cell walls]], and [[myeloperoxidase]] (used to generate toxic bacteria-killing substances).<ref name=USC /> In addition, secretions from the [[azurophilic granules|primary granules]] of neutrophils stimulate the phagocytosis of [[Immunoglobulin G|IgG]] antibody-coated bacteria.<ref name="pmid18787642">{{cite journal | vauthors = Soehnlein O, Kai-Larsen Y, Frithiof R, Sorensen OE, Kenne E, Scharffetter-Kochanek K, Eriksson EE, Herwald H, Agerberth B, Lindbom L | display-authors = 6 | title = Neutrophil primary granule proteins HBP and HNP1-3 boost bacterial phagocytosis by human and murine macrophages | journal = The Journal of Clinical Investigation | volume = 118 | issue = 10 | pages = 3491–502 | date = October 2008 | pmid = 18787642 | pmc = 2532980 | doi = 10.1172/JCI35740 }}</ref> The secondary granules contain compounds that are involved in the formation of toxic [[oxygen compounds]], lysozyme, and [[lactoferrin]] (used to take essential [[iron]] from bacteria).<ref name=USC /> [[Neutrophil extracellular traps]] (NETs) comprise a web of fibers composed of [[chromatin]] and [[serine protease]]s that trap and kill microbes extracellularly. Trapping of bacteria is a particularly important role for NETs in sepsis, where NET are formed within blood vessels.<ref name="NatMed">{{cite journal | vauthors = Clark SR, Ma AC, Tavener SA, McDonald B, Goodarzi Z, Kelly MM, Patel KD, Chakrabarti S, McAvoy E, Sinclair GD, Keys EM, Allen-Vercoe E, Devinney R, Doig CJ, Green FH, Kubes P | display-authors = 6 | title = Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood | journal = Nature Medicine | volume = 13 | issue = 4 | pages = 463–9 | date = April 2007 | pmid = 17384648 | doi = 10.1038/nm1565 | s2cid = 22372863 }}</ref>

===Eosinophils===
{{main|Eosinophil}}
Eosinophils also have kidney-shaped [[lobation|lobed]] nuclei (two to four lobes). The number of granules in an eosinophil can vary because they have a tendency to [[degranulation|degranulate]] while in the blood stream.<ref name=hess>{{cite web |title=Segmented Eosinophil |last=Hess |first=Charles E. |name-list-style=vanc |url=http://www.hsc.virginia.edu/internet/hematology/HessEDD/BenignHematologicDisorders/normal-hematopoietic-cells/Segmented-eosinophil.cfm |access-date=2009-04-10 |publisher=University of Virginia Health System |archive-date=2009-08-13 |archive-url=https://web.archive.org/web/20090813123547/http://www.hsc.virginia.edu/internet/hematology/HessEDD/BenignHematologicDisorders/normal-hematopoietic-cells/Segmented-eosinophil.cfm }}</ref> Eosinophils play a crucial part in the killing of parasites (e.g., enteric nematodes) because their granules contain a unique, toxic basic protein and cationic protein (e.g., [[cathepsin]]<ref name=USC>{{cite web| last = Mayer| first = Gene|title=Immunology — Chapter One: Innate (non-specific) Immunity| work = Microbiology and Immunology On-Line Textbook| publisher = USC School of Medicine| year = 2006|url=http://pathmicro.med.sc.edu/ghaffar/innate.htm| access-date = November 12, 2008}}</ref>);<ref name=tex>{{cite book | editor-last = Baron | editor-first = Samuel | title = Medical Microbiology | chapter = Immunology Overview | publisher = University of Texas Medical Branch at Galveston | year = 1996 | url = https://www.ncbi.nlm.nih.gov/books/NBK7795/ | isbn = 978-0-9631172-1-2 | edition = 4th | pmid = 21413267 |id=NBK7795}}</ref> receptors that bind to [[IgG]] and [[IgA]] are used to help with this task.<ref>{{cite journal | author1= Kelly D. Stone | author2= Calman Prussin | author3= Dean D. Metcalfe | title = IgE, Mast Cells, Basophils, and Eosinophils | journal = Allergy and Clincical Immunology | volume = 125 | issue = 2 | pages = S73-80 | date = February 2010 | pmc = 2847274 | doi = 10.1016/j.jaci.2009.11.017 | pmid= 20176269 }}</ref> These cells also have a limited ability to participate in phagocytosis,<ref name=Campbell>{{harvnb|Campbell|Reece|2002|p=903}}</ref> they are professional antigen-presenting cells, they regulate other immune cell functions (e.g., [[CD4+ T cell]], [[dendritic cell]], [[B cell]], [[mast cell]], [[neutrophil]], and [[basophil]] functions),<ref>{{cite journal | vauthors = Akuthota P, Wang HB, Spencer LA, Weller PF | title = Immunoregulatory roles of eosinophils: a new look at a familiar cell | journal = Clinical and Experimental Allergy | volume = 38 | issue = 8 | pages = 1254–63 | date = August 2008 | pmid = 18727793 | pmc = 2735457 | doi = 10.1111/j.1365-2222.2008.03037.x }}</ref> they are involved in the destruction of tumor cells,<ref name=hess /> and they promote the repair of damaged tissue.<ref>{{cite journal | vauthors = Kariyawasam HH, Robinson DS | title = The eosinophil: the cell and its weapons, the cytokines, its locations | journal = Seminars in Respiratory and Critical Care Medicine | volume = 27 | issue = 2 | pages = 117–27 | date = April 2006 | pmid = 16612762 | doi = 10.1055/s-2006-939514 }}</ref> A polypeptide called [[interleukin-5]] interacts with eosinophils and causes them to grow and differentiate; this polypeptide is produced by basophils and by T-helper 2 cells (TH2).<ref name=tex />

=== Basophils ===
{{main|Basophil}}
Basophils are one of the least abundant cells in [[bone marrow]] and [[blood]] (occurring at less than two percent of all cells). Like neutrophils and eosinophils, they have lobed [[Cell nucleus|nuclei]]; however, they have only two lobes, and the [[chromatin]] filaments that connect them are not very visible. Basophils have receptors that can bind to [[IgE]], [[Immunoglobulin G|IgG]], [[complement system|complement]], and [[histamine]]. The [[cytoplasm]] of basophils contains a varied amount of granules; these granules are usually numerous enough to partially conceal the nucleus. [[Granule (cell biology)|Granule]] contents of basophils are abundant with histamine, [[heparin]], [[chondroitin sulfate]], [[peroxidase]], [[platelet-activating factor]], and other substances.<ref>{{cite journal |vauthors=Hellman L, Akula S, Fu Z, Wernersson S |title=Mast Cell and Basophil Granule Proteases — In Vivo Targets and Function |journal=Front Immunol |volume=13 |issue= |article-number=918305 |date=2022 |pmid=35865537 |pmc=9294451 |doi=10.3389/fimmu.2022.918305 |doi-access=free}}</ref>

When an infection occurs, mature basophils will be released from the bone marrow and travel to the site of infection.<ref>{{cite web |url=http://www.hsc.virginia.edu/internet/hematology/HessEDD/BenignHematologicDisorders/normal-hematopoietic-cells/Mature-basophil.cfm |title=Mature Basophil |access-date=2009-04-10 |last=Hess |first=Charles E. |name-list-style=vanc |publisher=University of Virginia Health System |archive-date=2009-08-13 |archive-url=https://web.archive.org/web/20090813123542/http://www.hsc.virginia.edu/internet/hematology/HessEDD/BenignHematologicDisorders/normal-hematopoietic-cells/Mature-basophil.cfm }}</ref> When basophils are injured, they will release histamine, which contributes to the [[inflammatory response]] that helps fight invading organisms. Histamine causes dilation and increased permeability of [[capillaries]] close to the basophil. Injured basophils and other [[leukocytes]] will release another substance called [[prostaglandins]] that contributes to an increased blood flow to the site of infection. Both of these mechanisms allow blood-clotting elements to be delivered to the infected area (this begins the recovery process and blocks the travel of [[microbes]] to other parts of the body). Increased permeability of the inflamed tissue also allows for more [[phagocyte]] migration to the site of infection so that they can consume microbes.<ref name="Campbell" />

===Mast cells===
{{Hatnote|See article: [[Mast cell]]}}
Mast cells are a type of granulocyte that are present in tissues;<ref name="Granulocyte 2017 review" /> they mediate host defense against [[pathogen]]s (e.g., [[parasite]]s) and [[allergic reaction]]s, particularly [[anaphylaxis]].<ref name="Granulocyte 2017 review" /> Mast cells are also involved in mediating [[inflammation]] and [[autoimmunity]] as well as mediating and regulating [[neuroimmune system]] responses.<ref name="Granulocyte 2017 review" /><ref>{{cite journal | vauthors = Lee DM, Friend DS, Gurish MF, Benoist C, Mathis D, Brenner MB | title = Mast cells: a cellular link between autoantibodies and inflammatory arthritis | journal = Science | volume = 297 | issue = 5587 | pages = 1689–92 | date = September 2002 | pmid = 12215644 | doi = 10.1126/science.1073176 | bibcode = 2002Sci...297.1689L | s2cid = 38504601 }}</ref><ref name="Mast cell neuroimmmune system">{{cite journal | vauthors = Polyzoidis S, Koletsa T, Panagiotidou S, Ashkan K, Theoharides TC | title = Mast cells in meningiomas and brain inflammation | journal = Journal of Neuroinflammation | volume = 12 | issue = 1 | page = 170 | date = September 2015 | pmid = 26377554 | pmc = 4573939 | doi = 10.1186/s12974-015-0388-3 | quote = MCs originate from a bone marrow progenitor and subsequently develop different phenotype characteristics locally in tissues. Their range of functions is wide and includes participation in allergic reactions, innate and adaptive immunity, inflammation, and autoimmunity [34]. In the human brain, MCs can be located in various areas, such as the pituitary stalk, the pineal gland, the area postrema, the choroid plexus, thalamus, hypothalamus, and the median eminence [35]. In the meninges, they are found within the dural layer in association with vessels and terminals of meningeal nociceptors [36]. MCs have a distinct feature compared to other hematopoietic cells in that they reside in the brain [37]. MCs contain numerous granules and secrete an abundance of prestored mediators such as corticotropin-releasing hormone (CRH), neurotensin (NT), substance P (SP), tryptase, chymase, vasoactive intestinal peptide (VIP), vascular endothelial growth factor (VEGF), TNF, prostaglandins, leukotrienes, and varieties of chemokines and cytokines some of which are known to disrupt the integrity of the blood-brain barrier (BBB) [38–40].<br /><br />They key role of MCs in inflammation [34] and in the disruption of the BBB [41–43] suggests areas of importance for novel therapy research. Increasing evidence also indicates that MCs participate in neuroinflammation directly [44–46] and through microglia stimulation [47], contributing to the pathogenesis of such conditions such as headaches, [48] autism [49], and chronic fatigue syndrome [50]. In fact, a recent review indicated that peripheral inflammatory stimuli can cause microglia activation [51], thus possibly involving MCs outside the brain. | doi-access = free }}</ref>

==Development==
Granulocytes are derived from stem cells residing in the bone marrow. The differentiation of these stem cells from multipotent [[hematopoietic stem cell]] into granulocytes is termed [[granulopoiesis]]. Multiple intermediate cell types exist in this differentiation process, including [[myeloblast]]s and [[promyelocyte]]s.<ref>{{cite journal |vauthors=Calzetti F, Finotti G, Cassatella MA |title=Current knowledge on the early stages of human neutropoiesis |journal=Immunol Rev |volume=314 |issue=1 |pages=111–124 |date=March 2023 |pmid=36484356 |doi=10.1111/imr.13177 }}</ref>

== Function ==
===Granule contents===
Examples of toxic materials produced or released by [[degranulation]] by granulocytes on the ingestion of microorganisms are:
* [[Antimicrobial]] agents ([[Defensin]]s and [[Eosinophil cationic protein]])
* [[Enzyme]]s
** [[Lysozyme]]: dissolves cell walls of some [[gram-positive bacteria]]
** [[Acid hydrolase]]s: further digest bacteria
* Low pH [[Vesicle (biology)|vesicles]] (3.5-4.0)
* Toxic [[nitrogen]] oxides ([[nitric oxide]])
* Toxic [[oxygen]]-derived products (e.g., [[superoxide]], [[hydrogen peroxide]], [[hydroxy radical]]s, [[singlet oxygen]], [[hypohalite]])

==Clinical significance==
'''Granulocytopenia''' is an abnormally low concentration of granulocytes in the blood. This condition reduces the body's resistance to many infections. Closely related terms include [[agranulocytosis]] (etymologically, "no granulocytes at all"; clinically, granulocyte levels less than 5% of normal) and [[neutropenia]] (deficiency of [[neutrophil granulocyte]]s). Granulocytes live only one to two days in circulation (four days in [[spleen]] or other tissue), so [[Blood transfusion|transfusion]] of granulocytes as a therapeutic strategy would confer a very short-lasting benefit. In addition, there are many complications associated with such a procedure.

There is usually a granulocyte [[Chemotaxis|chemotactic]] defect in individuals suffering from [[type 1 diabetes mellitus]].

Research suggests giving granulocyte transfusions to prevent infections decreased the number of people who had a bacterial or fungal infection in the blood.<ref>{{cite journal | vauthors = Estcourt LJ, Stanworth S, Doree C, Blanco P, Hopewell S, Trivella M, Massey E | title = Granulocyte transfusions for preventing infections in people with neutropenia or neutrophil dysfunction | journal = The Cochrane Database of Systematic Reviews | issue = 6 | article-number = CD005341 | date = June 2015 | volume = 2018 | pmid = 26118415 | pmc = 4538863 | doi = 10.1002/14651858.cd005341.pub3 }}</ref> Further research suggests participants receiving therapeutic [[granulocyte transfusion]]s show no difference in clinical reversal of concurrent infection.<ref>{{cite journal | vauthors = Estcourt LJ, Stanworth SJ, Hopewell S, Doree C, Trivella M, Massey E | title = Granulocyte transfusions for treating infections in people with neutropenia or neutrophil dysfunction | journal = The Cochrane Database of Systematic Reviews | volume = 4 | article-number = CD005339 | date = April 2016 | issue = 7 | pmid = 27128488 | pmc = 4930145 | doi = 10.1002/14651858.cd005339.pub2}}</ref>

==Additional images==
<gallery>
Image:Hematopoiesis (human) diagram en.svg|Hematopoiesis
</gallery>

== See also ==
* [[Blood count]]
* [[Haematopoiesis]]
* [[Immune system]]
* [[Innate immune system]]
* [[Trogocytosis]]
* [[White blood cell]]

== References ==
{{Reflist|35em}}

==Bibliography==
{{refbegin}}
* {{cite book | vauthors = Campbell NA, Reece JB | title = Biology | edition = 6th | publisher = Pearson Education | date = 2002 | isbn = 978-0-8053-6624-2 | url-access = registration | url = https://archive.org/details/biologyc00camp }}
* {{cite book | vauthors = Delves PJ, Martin SJ, Burton DR, Roit IM | title = Roitt's Essential Immunology | edition = 11th | publisher = Blackwell | date = 2006 | isbn = 978-1-4051-3603-7 }}
* {{cite book | vauthors = Ernst JD, Stendahl O | title = Phagocytosis of Bacteria and Bacterial Pathogenicity | publisher = Cambridge University Press | date = 2006 | isbn = 0-521-84569-6 | url = http://www.cambridge.org/9780521845694 }}
* {{cite book | vauthors = Hoffbrand AV, Pettit JE, Moss PA | title = Essential Haematology | edition = 4th | publisher = Blackwell Science | date = 2005 | isbn = 978-0-632-05153-3 }}
* {{cite book | veditors = Paoletti R, Notario A, Ricevuti G | title = Phagocytes: Biology, Physiology, Pathology, and Pharmacotherapeutics | publisher = The New York Academy of Sciences | date = 1997 | isbn = 978-1-57331-102-1 }}
* {{cite book | veditors = Robinson JP, Babcock GF | title = Phagocyte Function —A guide for research and clinical evaluation | publisher = Wiley–Liss | date = 1998 | isbn = 978-0-471-12364-4 | url-access = registration | url = https://archive.org/details/phagocytefunctio0000unse }}
* {{cite book | last = Sompayrac |first=L | title = How the Immune System Works | edition = 3rd | publisher = Blackwell | date = 2008 | isbn = 978-1-4051-6221-0}}
{{refend}}

== External links ==
* {{Commons-inline}}

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[[Category:Leukocytes]]

Granulocyte - Revision history

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