Eczema pathophysiology: Difference between revisions
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*Affected [[skin]] involves the uptake of [[antigens]] and [[allergens]]by the [[epidermal]] [[dendritic cells]], [[dermal]] [[dendritic cells]], and [[Langerhan cells]]. | *Affected [[skin]] involves the uptake of [[antigens]] and [[allergens]]by the [[epidermal]] [[dendritic cells]], [[dermal]] [[dendritic cells]], and [[Langerhan cells]]. | ||
*[[Sensory nerves]] are activated by the released [[cytokines]] interleukins 4,13 and 31 ([[IL-4]], [[IL-13]], and [[IL-31]]), which are responsible for the [[pruritic]] sensation. | *[[Sensory nerves]] are activated by the released [[cytokines]] interleukins 4,13 and 31 ([[IL-4]], [[IL-13]], and [[IL-31]]), which are responsible for the [[pruritic]] sensation. | ||
*As the event becomes chronic, an increased expression of [[keratinocyte]] and [[Th-cell]]-derived [[cytokines]] is achieved, with more [[pruritogens]] contributing to [[itch]] sensation. | *As the event becomes chronic, an increased expression of [[keratinocyte]] and [[Th-cell]]-derived [[cytokines]] is achieved, with more [[pruritogens]] contributing to [[itch]] sensation. <ref name="pmid27212086">{{cite journal| author=Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G | display-authors=etal| title=The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves. | journal=J Allergy Clin Immunol | year= 2016 | volume= 138 | issue= 2 | pages= 500-508.e24 | pmid=27212086 | doi=10.1016/j.jaci.2016.02.020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27212086 }} </ref> | ||
* There are two main theories on the existence of [[atopic dermatitis]], also known as [[atopic eczema]] - the ''inside-out hypothesis'', and the ''outside-in hypothesis''.<ref name="pmid26761930">{{cite journal| author=Silverberg NB, Silverberg JI| title=Inside out or outside in: does atopic dermatitis disrupt barrier function or does disruption of barrier function trigger atopic dermatitis? | journal=Cutis | year= 2015 | volume= 96 | issue= 6 | pages= 359-61 | pmid=26761930 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26761930 }} </ref> | * There are two main theories on the existence of [[atopic dermatitis]], also known as [[atopic eczema]] - the ''inside-out hypothesis'', and the ''outside-in hypothesis''.<ref name="pmid26761930">{{cite journal| author=Silverberg NB, Silverberg JI| title=Inside out or outside in: does atopic dermatitis disrupt barrier function or does disruption of barrier function trigger atopic dermatitis? | journal=Cutis | year= 2015 | volume= 96 | issue= 6 | pages= 359-61 | pmid=26761930 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26761930 }} </ref> | ||
* ''Inside-out hypothesis'' | * ''Inside-out hypothesis'' | ||
Revision as of 14:46, 21 June 2022
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
The mechanism of disease of eczema involves a complex interplay of abnormalities of skin microbiomes, a dysfunction in the epidermal barrier, and an immune dysregulation. [1] There are two main theories on the existence of atopic dermatitis, also known as atopic eczema - the inside-out hypothesis, and the outside-in hypothesis.
Pathophysiology
- Affected skin involves the uptake of antigens and allergensby the epidermal dendritic cells, dermal dendritic cells, and Langerhan cells.
- Sensory nerves are activated by the released cytokines interleukins 4,13 and 31 (IL-4, IL-13, and IL-31), which are responsible for the pruritic sensation.
- As the event becomes chronic, an increased expression of keratinocyte and Th-cell-derived cytokines is achieved, with more pruritogens contributing to itch sensation. [1]
- There are two main theories on the existence of atopic dermatitis, also known as atopic eczema - the inside-out hypothesis, and the outside-in hypothesis.[2]
- Inside-out hypothesis
- This hypothesis denotes that some allergic triggers weaken the skin barrier that leads to more introduction of allergens to the area, causing more inflammatory reaction.[2]
- Outside-in hypothesis
- This hypothesis suggests that an impairment of the skin barrier should occur first before the onset of atopic dermatitis.
- This involves the down-regulation of filaggrin genes (FLG) responsible for maintenance of the proper function of skin barrier.[2] [3]
References
- ↑ 1.0 1.1 Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G; et al. (2016). "The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves". J Allergy Clin Immunol. 138 (2): 500–508.e24. doi:10.1016/j.jaci.2016.02.020. PMID 27212086.
- ↑ 2.0 2.1 2.2 Silverberg NB, Silverberg JI (2015). "Inside out or outside in: does atopic dermatitis disrupt barrier function or does disruption of barrier function trigger atopic dermatitis?". Cutis. 96 (6): 359–61. PMID 26761930.
- ↑ Leung DY, Guttman-Yassky E (2014). "Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches". J Allergy Clin Immunol. 134 (4): 769–79. doi:10.1016/j.jaci.2014.08.008. PMC 4186710. PMID 25282559.