Allergic conjunctivitis pathophysiology: Difference between revisions

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[[Degranulation]] of [[mast]] [[cells]] activates [[vascular]] [[endothelial]] [[cells]] to express [[adhesion]] molecules such as [[intercellular]] [[adhesion]] molecule ([[ICAM]]), [[vascular]] [[cell]] [[adhesion]] molecule ([[VCAM]]) and release [[chemokines]] like regulated upon activation normal [[T]] [[cells]] expressed and secreted ([[RANTES]]), [[monocyte]] [[chemoattractant]] [[protein]] ([[MCP]]), [[Interleukin]] (IL)-8, [[eotaxin]], [[macrophage]] [[inflammatory]] [[protein]] ([[MIP]])-1 alpha.
[[Degranulation]] of [[mast]] [[cells]] activates [[vascular]] [[endothelial]] [[cells]] to express [[adhesion]] molecules such as [[intercellular]] [[adhesion]] molecule ([[ICAM]]), [[vascular]] [[cell]] [[adhesion]] molecule ([[VCAM]]) and release [[chemokines]] like regulated upon activation normal [[T]] [[cells]] expressed and secreted ([[RANTES]]), [[monocyte]] [[chemoattractant]] [[protein]] ([[MCP]]), [[Interleukin]] (IL)-8, [[eotaxin]], [[macrophage]] [[inflammatory]] [[protein]] ([[MIP]])-1 alpha.
                                                   ↓
                                                   ↓
Triggers the recruitment of [[inflammatory]] cells in the [[conjunctival]] [[mucosa]], which mediate the [[ocular]] late-phase reaction<ref name="pmid12044269">{{cite journal| author=Leonardi A| title=The central role of conjunctival mast cells in the pathogenesis of ocular allergy. | journal=Curr Allergy Asthma Rep | year= 2002 | volume= 2 | issue= 4 | pages= 325-31 | pmid=12044269 | doi=10.1007/s11882-002-0061-7 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12044269  }} </ref>.


==References==
==References==

Revision as of 17:23, 20 August 2022

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sujaya Chattopadhyay, M.D.[2]

Overview

The ocular allergic response is a cascade of events that is coordinated by mast cells.[1]

Pathophysiology

Allergic conjunctivitis is the manifestation of a predominantly IgE-mediated hypersensitivity reaction[2].

Stimulated mast cells release increased amounts of tryptase, histamine, prostaglandins and leukotrienes in tears. This is the immediate response, which lasts for the initial 20-30 min.

Degranulation of mast cells activates vascular endothelial cells to express adhesion molecules such as intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) and release chemokines like regulated upon activation normal T cells expressed and secreted (RANTES), monocyte chemoattractant protein (MCP), Interleukin (IL)-8, eotaxin, macrophage inflammatory protein (MIP)-1 alpha.

Triggers the recruitment of inflammatory cells in the conjunctival mucosa, which mediate the ocular late-phase reaction[3].

References

  1. Liu G, Keane-Myers A, Miyazaki D, Tai A, Ono SJ (1999). "Molecular and cellular aspects of allergic conjunctivitis". Chem. Immunol. Chemical Immunology and Allergy. 73: 39–58. doi:10.1159/000058748. ISBN 3-8055-6893-2. PMID 10590573.
  2. La Rosa M, Lionetti E, Reibaldi M, Russo A, Longo A, Leonardi S; et al. (2013). "Allergic conjunctivitis: a comprehensive review of the literature". Ital J Pediatr. 39: 18. doi:10.1186/1824-7288-39-18. PMC 3640929. PMID 23497516.
  3. Leonardi A (2002). "The central role of conjunctival mast cells in the pathogenesis of ocular allergy". Curr Allergy Asthma Rep. 2 (4): 325–31. doi:10.1007/s11882-002-0061-7. PMID 12044269.

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