Granulocyte

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Polymorphonuclear leukocyte
)
Granulocyte
A basophilic granulocyte.
Details
SystemImmune system
Identifiers
MeSHD006098
FMA62854
Anatomical terms of microanatomy

Granulocytes are cells in the innate immune system characterized by the presence of specific granules in their cytoplasm.[1] Such granules distinguish them from the various agranulocytes. All myeloblastic granulocytes are polymorphonuclear, that is, they have varying shapes (morphology) of the 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",[2] the most abundant of the granulocytes; the other types (eosinophils, basophils, and mast cells) have varying morphology. Granulocytes are produced via granulopoiesis in the bone marrow.

Types

There are four types of granulocytes (full name polymorphonuclear granulocytes):[3]

Except for the mast cells, their names are derived from their

neutrophil granulocyte, which has neutrally staining cytoplasmic granules.[citation needed
]

Neutrophils

erythrocytes), the intra-cellular granules are visible in the cytoplasm (Giemsa-stained
high magnification)

Neutrophils are normally found in the bloodstream and are the most abundant type of phagocyte, constituting 60% to 65% of the total circulating white blood cells,[4] and consisting of two subpopulations: neutrophil-killers and neutrophil-cagers. One litre of human blood contains about five billion (5x109) neutrophils,[5] which are about 12–15 micrometres in diameter.[6] Once neutrophils have received the appropriate signals, it takes them about thirty minutes to leave the blood and reach the site of an infection.[7] Neutrophils do not return to the blood; they turn into pus cells and die.[7] Mature neutrophils are smaller than monocytes, and have a segmented 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 myelocytes and promyelocytes are released.[8]

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).[9] Neutrophils are professional

phagocytes:[10] they are ferocious eaters and rapidly engulf invaders coated with antibodies and 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.[11] Neutrophils can secrete products that stimulate monocytes and macrophages; these secretions increase phagocytosis and the formation of reactive oxygen compounds involved in intracellular killing.[12]

Neutrophils have two types of granules; primary (azurophilic) granules (found in young cells) and

primary granules of neutrophils stimulate the phagocytosis of IgG antibody-coated bacteria.[14] 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).[13] Neutrophil extracellular traps (NETs) comprise a web of fibers composed of chromatin and serine proteases 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.[15]

Eosinophils

Eosinophils also have kidney-shaped

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).[17]

Basophils

erythrocytes

Basophils are one of the least abundant cells in

IgE, IgG, 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 contents of basophils are abundant with histamine, heparin, chondroitin sulfate, peroxidase, platelet-activating factor, and other substances.[citation needed
]

When an infection occurs, mature basophils will be released from the bone marrow and travel to the site of infection.

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.[19]

Mast cells

Mast cells are a type of granulocyte that are present in tissues;

allergic reactions, particularly anaphylaxis.[3] Mast cells are also involved in mediating inflammation and autoimmunity as well as mediating and regulating neuroimmune system responses.[3][23][24]

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 myeloblasts and promyelocytes.[citation needed]

Function

Granule contents

Examples of toxic materials produced or released by degranulation by granulocytes on the ingestion of microorganisms are:

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

neutrophil granulocytes). Granulocytes live only one to two days in circulation (four days in spleen or other tissue), so 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

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.[25] Further research suggests participants receiving therapeutic granulocyte transfusions show no difference in clinical reversal of concurrent infection.[26]

Additional images

  • Hematopoiesis
    Hematopoiesis

See also

References

  1. .
  2. .
  3. ^ .
  4. on December 31, 2010. Retrieved March 28, 2009.
  5. ^ Hoffbrand p. 331
  6. ^ Abbas, Chapter 12, 5th Edition[full citation needed][page needed]
  7. ^ a b Sompayrac p. 18
  8. PMID 9853933
    .
  9. .
  10. ^ Robinson p. 187 and Ernst pp. 7–10
  11. ^ Paoletti p. 62
  12. PMID 17991288
    .
  13. ^ a b c Mayer, Gene (2006). "Immunology — Chapter One: Innate (non-specific) Immunity". Microbiology and Immunology On-Line Textbook. USC School of Medicine. Retrieved November 12, 2008.
  14. PMID 18787642
    .
  15. .
  16. ^ a b Hess CE. "Segmented Eosinophil". University of Virginia Health System. Archived from the original on 2009-08-13. Retrieved 2009-04-10.
  17. ^ .
  18. .
  19. ^ a b Campbell p. 903
  20. PMID 18727793
    .
  21. .
  22. ^ Hess CE. "Mature Basophil". University of Virginia Health System. Archived from the original on 2009-08-13. Retrieved 2009-04-10.
  23. S2CID 38504601
    .
  24. . 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].

    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.
  25. .
  26. .

Bibliography

External links