Eosinophil

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Eosinophil granulocyte
)
Eosinophil
blood smear. Red blood cells surround the eosinophil, two platelets at the top left corner.
Details
Pronunciation/ˌˈsɪnəfɪl/)[1]
SystemImmune system
Identifiers
MeSHD004804
THH2.00.04.1.02017
FMA62861
Anatomical terms of microanatomy]

Eosinophils, sometimes called eosinophiles or, less commonly, acidophils, are a variety of

hematopoiesis in the bone marrow before migrating into blood, after which they are terminally differentiated and do not multiply.[3]

These

plasminogen, and major basic protein. These mediators are released by a process called degranulation following activation of the eosinophil, and are toxic
to both parasite and host tissues.

In normal individuals, eosinophils make up about 1–3% of white blood cells, and are about 12–17

lymph nodes, but not in the lungs, skin, esophagus, or some other internal organs[vague] under normal conditions. The presence of eosinophils in these latter organs is associated with disease. For instance, patients with eosinophilic asthma have high levels of eosinophils that lead to inflammation and tissue damage, making it more difficult for patients to breathe.[6][7] Eosinophils persist in the circulation for 8–12 hours, and can survive in tissue for an additional 8–12 days in the absence of stimulation.[8] Pioneering work in the 1980s elucidated that eosinophils were unique granulocytes, having the capacity to survive for extended periods of time after their maturation as demonstrated by ex-vivo culture experiments.[9]

Development

Blood cell lineage

Interleukin-13, another TH2 cytokine, primes eosinophilic exit from the bone marrow by lining vessel walls with adhesion molecules such as VCAM-1 and ICAM-1.[6]
When eosinophils are activated, they undergo cytolysis, where the breaking of the cell releases eosinophilic granules found in extracellular DNA traps.[6] High concentrations of these DNA traps are known to cause cellular damage, as the granules they contain are responsible for the ligand-induced secretion of eosinophilic toxins which cause structural damage.[6] There is evidence to suggest that eosinophil granule protein expression is regulated by the non-coding RNA EGOT.[13]

Function

Histology of an eosinophil within epithelium, characterized by its bilobed nucleus despite scant visible eosinophilic cytoplasm.

Following activation, eosinophils effector functions include production of the following:

There are also eosinophils that play a role in fighting viral infections, which is evident from the abundance of

neoplasia.[21] They have also been implicated in antigen presentation to T cells.[22]

Eosinophils are responsible for tissue damage and inflammation in many diseases, including asthma.[6][7] High levels of interleukin-5 has been observed to up regulate the expression of adhesion molecules, which then facilitate the adhesion of eosinophils to endothelial cells, thereby causing inflammation and tissue damage.[7]

An accumulation of eosinophils in the nasal mucosa is considered a major diagnostic criterion for allergic rhinitis (nasal allergies).

Granule proteins

Following activation by an immune stimulus, eosinophils degranulate to release an array of cytotoxic granule cationic proteins that are capable of inducing tissue damage and dysfunction.[23] These include:

Major basic protein, eosinophil peroxidase, and eosinophil cationic protein are toxic to many tissues.[21] Eosinophil cationic protein and eosinophil-derived neurotoxin are ribonucleases with antiviral activity.[24] Major basic protein induces mast cell and basophil degranulation, and is implicated in peripheral nerve remodelling.[25][26] Eosinophil cationic protein creates toxic pores in the membranes of target cells, allowing potential entry of other cytotoxic molecules to the cell,[27] can inhibit proliferation of T cells, suppress antibody production by B cells, induce degranulation by mast cells, and stimulate fibroblast cells to secrete mucus and glycosaminoglycan.[28] Eosinophil peroxidase forms reactive oxygen species and reactive nitrogen intermediates that promote oxidative stress in the target, causing cell death by apoptosis and necrosis.[21]

Clinical significance

Eosinophilia

An increase in eosinophils, i.e., the presence of more than 500 eosinophils/microlitre of blood is called an

toxic oil syndrome
in Spain in 1981.

Reference ranges for blood tests of white blood cells, comparing eosinophil granulocyte amount (shown in light red) with other cells

Eosinophils play an important role in asthma as the number of accumulated eosinophils corresponds to the severity of asthmatic reaction.[7] Eosinophilia in mice models are shown to be associated with high interleukin-5 levels.[7] Furthermore, mucosal bronchial biopsies conducted on patients with diseases such as asthma have been found to have higher levels of interleukin-5 leading to higher levels of eosinophils.[7] The infiltration of eosinophils at these high concentrations causes an inflammatory reaction.[7] This ultimately leads to airway remodelling and difficulty of breathing.[7]

Eosinophils can also cause tissue damage in the lungs of asthmatic patients.[7] High concentrations of eosinophil major basic protein and eosinophil-derived neurotoxin that approach cytotoxic levels are observed at degranulation sites in the lungs as well as in the asthmatic sputum.[7]

Treatment

Treatments used to combat autoimmune diseases and conditions caused by eosinophils include:

Monoclonal antibodies such as dupilumab and lebrikizumab target IL-13 and its receptor, which reduces eosinophilic inflammation in patients with asthma due to lowering the number of adhesion molecules present for eosinophils to bind to, thereby decreasing inflammation.[29][30] Mepolizumab and benralizumab are other treatment options that target the alpha subunit of the IL-5 receptor, thereby inhibiting its function and reducing the number of developing eosinophils as well as the number of eosinophils leading to inflammation through antibody-dependent cell-mediated cytotoxicity and eosinophilic apoptosis.[31][32]

Animal studies

Within the fat (adipose) tissue of CCR2 deficient mice, there is an increased number of eosinophils, greater alternative macrophage activation, and a propensity towards type 2 cytokine expression. Furthermore, this effect was exaggerated when the mice became obese from a high fat diet.[33] Mouse models of eosinophilia from mice infected with T. canis showed an increase in IL-5 mRNA in mice spleen.[7] Mouse models of asthma from OVA show a higher TH2 response.[6] When mice are administered IL-12 to induce the TH1 response, the TH2 response becomes suppressed, showing that mice without TH2 cytokines are significantly less likely to express asthma symptoms.[6]

See also

References

  1. ^ "eosinophil - Definition of eosinophil in English by Oxford Dictionaries". Oxford Dictionaries - English. Archived from the original on 8 February 2018. Retrieved 27 March 2018.
  2. ^ "What is an Eosinophil? | Definition & Function | CCED". www.cincinnatichildrens.org. Retrieved 14 June 2018.
  3. ^
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  33. PMID 25934927. Archived from the original
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