# Allergic inflammation

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**Allergic inflammation** is an important pathophysiological feature of several [disabilities](/source/Disabilities) or [medical conditions](/source/Medical_conditions) including allergic [asthma](/source/Asthma), [atopic dermatitis](/source/Atopic_dermatitis), allergic [rhinitis](/source/Rhinitis) and several [ocular](/source/Human_eye) allergic diseases. Allergic reactions may generally be divided into two components; the early phase reaction, and the late phase reaction. While the contribution to the development of symptoms from each of the phases varies greatly between diseases, both are usually present and provide us a framework for understanding allergic disease.[1][2][3][4]

The early phase of the allergic reaction typically occurs within minutes, or even seconds, following [allergen](/source/Allergen) exposure and is also commonly referred to as the immediate allergic reaction or as a Type I allergic reaction.[5] The reaction is caused by the release of [histamine](/source/Histamine) and [mast cell](/source/Mast_cell) granule proteins by a process called [degranulation](/source/Degranulation), as well as the production of [leukotrienes](/source/Leukotrienes), [prostaglandins](/source/Prostaglandins) and [cytokines](/source/Cytokines), by mast cells following the cross-linking of allergen specific [IgE](/source/IgE) molecules bound to mast cell [FcεRI](/source/Fc%CE%B5RI) receptors.[3] These mediators affect [nerve cells](/source/Nerve_cells) causing itching,[6] [smooth muscle](/source/Smooth_muscle) cells causing contraction (leading to the airway narrowing seen in allergic asthma),[4] [goblet cells](/source/Goblet_cells) causing mucus production,[1] and [endothelial](/source/Endothelial) cells causing [vasodilatation](/source/Vasodilator) and [edema](/source/Edema).[6]

The late phase of a Type 1 reaction (which develops 8–12 hours and is mediated by mast cells)[5] should not be confused with delayed hypersensitivity Type IV allergic reaction (which takes 48–72 hours to develop and is mediated by T cells).[7] The products of the early phase reaction include [chemokines](/source/Chemokines) and molecules that act on endothelial cells and cause them to express [Intercellular adhesion molecule](/source/Intercellular_adhesion_molecule) (such as [vascular cell adhesion molecule](/source/Cell_adhesion_molecule) and [selectins](/source/Selectins)), which together result in the recruitment and activation of [leukocytes](/source/Leukocytes) from the blood into the site of the allergic reaction.[3] Typically, the infiltrating cells observed in allergic reactions contain a high proportion of [lymphocytes](/source/Lymphocytes), and especially, of [eosinophils](/source/Eosinophils). The recruited eosinophils will degranulate releasing a number of [cytotoxic](/source/Cytotoxic) molecules (including [Major Basic Protein](/source/Major_Basic_Protein) and [eosinophil peroxidase](/source/Eosinophil_peroxidase)) as well as produce a number of cytokines such as [IL-5](/source/Interleukin_5).[8] The recruited [T-cells](/source/T-cells) are typically of the [Th2](/source/Th2) variety and the cytokines they produce lead to further recruitment of mast cells and eosinophils, and in [plasma cell](/source/Plasma_cell) isotype switching to IgE which will bind to the mast cell FcεRI receptors and prime the individual for further allergic responses.

## See also

- [Allergy](/source/Allergy)
- [Inflammation](/source/Inflammation)

### References

1. Fireman P (2003). ["Understanding asthma pathophysiology"](http://openurl.ingenta.com/content/nlm?genre=article&issn=1088-5412&volume=24&issue=2&spage=79&aulast=Fireman). *Allergy Asthma Proc*. **24** (2): 79–83. [PMID 12776439](https://pubmed.ncbi.nlm.nih.gov/12776439)

1. Leung DY (1998). "Molecular basis of allergic diseases". *Mol. Genet. Metab.*. **63** (3): 157–67. [doi:10.1006/mgme.1998.2682](https://doi.org/10.1006/mgme.1998.2682). [PMID 9608537](https://pubmed.ncbi.nlm.nih.gov/9608537)

1. Hansen I, Klimek L, Mösges R, Hörmann K (2004). "Mediators of inflammation in the early and the late phase of allergic rhinitis". *Curr Opin Allergy Clin Immunol*. **4** (3): 159–63. [doi:10.1097/00130832-200406000-00004](https://doi.org/10.1097/00130832-200406000-00004). [PMID 15126935](https://pubmed.ncbi.nlm.nih.gov/15126935)

1. Katelaris CH (2003). "Ocular allergy: implications for the clinical immunologist". *Ann. Allergy Asthma Immunol.*. **90** (6 Suppl 3): 23–7. [doi:10.1016/S1081-1206(10)61656-0](https://doi.org/10.1016/S1081-1206(10)61656-0). [PMID 12839109](https://pubmed.ncbi.nlm.nih.gov/12839109)

1. Janeway, Charles (2001). [*Immunobiology: the immune system in health and disease*](https://archive.org/details/immunobiology00char). 5th ed. New York: Garland. ISBN 0-8153-3642-X.

1. Trocme SD, Sra KK (2002). "Spectrum of ocular allergy". *Curr Opin Allergy Clin Immunol*. **2** (5): 423–7. [doi:10.1097/00130832-200210000-00010](https://doi.org/10.1097/00130832-200210000-00010). [PMID 12582327](https://pubmed.ncbi.nlm.nih.gov/12582327)

1. Hinshaw WD, Neyman GP, Olmstead SM. ["Hypersensitivity Reactions, Delayed"](http://emedicine.medscape.com/article/136118-overview). *EMedicine*

1. Rothenberg ME & Rothenberg, Marc E. (1998). "Eosinophilia". *N. Engl. J. Med.*. **338** (22): 1592–600. [doi:10.1056/NEJM199805283382206](https://doi.org/10.1056/NEJM199805283382206). [PMID 9603798](https://pubmed.ncbi.nlm.nih.gov/9603798)

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Adapted from the Wikipedia article [Allergic inflammation](https://en.wikipedia.org/wiki/Allergic_inflammation) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/Allergic_inflammation?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.