Aromatic oil from lavender as an atopic dermatitis suppressant
In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefo...
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description | In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines. |
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Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0296408</identifier><identifier>PMID: 38181031</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Acetates ; Acetic acid ; Advertising executives ; Air pollution ; Analgesics ; Animals ; Antigens ; Atopic dermatitis ; Carbazole ; Carbazoles ; Care and treatment ; Cell activation ; Cosmetics ; Cytokines ; Dendritic cells ; Dermatitis ; Dermatitis, Atopic - drug therapy ; Diagnosis ; Dioxins ; Essential oils ; Esters ; Folk medicine ; Food preservation ; Gene expression ; Health aspects ; Humans ; Hydrocarbons ; Immunoglobulins ; Itching ; Lavandula ; Lavandula angustifolia ; Lavender oil ; Linalool ; Linalyl acetate ; Metabolites ; Monoterpenes ; Mutation ; Nerves ; Neurotrophic factors ; Oils & fats ; Pollutants ; Proteins ; Reporter gene ; RNA ; Skin ; Skin diseases ; Tryptophan ; Ultraviolet radiation</subject><ispartof>PloS one, 2024-01, Vol.19 (1), p.e0296408-e0296408</ispartof><rights>Copyright: © 2024 Sato et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>COPYRIGHT 2024 Public Library of Science</rights><rights>2024 Sato et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Sato et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c696t-a3786bb2729b0175216ae9722b2208e7ac0b4538a9189b9f1fd02e02a3a3142b3</cites><orcidid>0000-0003-3736-1283 ; 0000-0001-6606-9105</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0296408&type=printable$$EPDF$$P50$$Gplos$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://journals.plos.org/plosone/article?id=10.1371/journal.pone.0296408$$EHTML$$P50$$Gplos$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,860,2096,2915,23845,27901,27902,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38181031$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sato, Haruna</creatorcontrib><creatorcontrib>Kato, Kosuke</creatorcontrib><creatorcontrib>Koreishi, Mayuko</creatorcontrib><creatorcontrib>Nakamura, Yoshimasa</creatorcontrib><creatorcontrib>Tsujino, Yoshio</creatorcontrib><creatorcontrib>Satoh, Ayano</creatorcontrib><title>Aromatic oil from lavender as an atopic dermatitis suppressant</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.</description><subject>Acetates</subject><subject>Acetic acid</subject><subject>Advertising executives</subject><subject>Air pollution</subject><subject>Analgesics</subject><subject>Animals</subject><subject>Antigens</subject><subject>Atopic dermatitis</subject><subject>Carbazole</subject><subject>Carbazoles</subject><subject>Care and treatment</subject><subject>Cell activation</subject><subject>Cosmetics</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Dermatitis</subject><subject>Dermatitis, Atopic - drug therapy</subject><subject>Diagnosis</subject><subject>Dioxins</subject><subject>Essential oils</subject><subject>Esters</subject><subject>Folk medicine</subject><subject>Food preservation</subject><subject>Gene expression</subject><subject>Health 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Yoshio</au><au>Satoh, Ayano</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aromatic oil from lavender as an atopic dermatitis suppressant</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2024-01-05</date><risdate>2024</risdate><volume>19</volume><issue>1</issue><spage>e0296408</spage><epage>e0296408</epage><pages>e0296408-e0296408</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>In atopic dermatitis (AD), nerves are abnormally stretched near the surface of the skin, making it sensitive to itching. Expression of neurotrophic factor Artemin (ARTN) involved in such nerve stretching is induced by the xenobiotic response (XRE) to air pollutants and UV radiation products. Therefore, AD can be monitored by the XRE response. Previously, we established a human keratinocyte cell line stably expressing a NanoLuc reporter gene downstream of XRE. We found that 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan metabolite and known inducer of the XRE, increased reporter and Artemin mRNA expression, indicating that FICZ-treated cells could be a model for AD. Lavender essential oil has been used in folk medicine to treat AD, but the scientific basis for its use is unclear. In the present study, we investigated the efficacy of lavender essential oil and its major components, linalyl acetate and linalool, to suppress AD and sensitize skin using the established AD model cell line, and keratinocyte and dendritic cell activation assays. Our results indicated that lavender essential oil from L. angustifolia and linalyl acetate exerted a strong AD inhibitory effect and almost no skin sensitization. Our model is useful in that it can circumvent the practice of using animal studies to evaluate AD medicines.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>38181031</pmid><doi>10.1371/journal.pone.0296408</doi><tpages>e0296408</tpages><orcidid>https://orcid.org/0000-0003-3736-1283</orcidid><orcidid>https://orcid.org/0000-0001-6606-9105</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Acetates Acetic acid Advertising executives Air pollution Analgesics Animals Antigens Atopic dermatitis Carbazole Carbazoles Care and treatment Cell activation Cosmetics Cytokines Dendritic cells Dermatitis Dermatitis, Atopic - drug therapy Diagnosis Dioxins Essential oils Esters Folk medicine Food preservation Gene expression Health aspects Humans Hydrocarbons Immunoglobulins Itching Lavandula Lavandula angustifolia Lavender oil Linalool Linalyl acetate Metabolites Monoterpenes Mutation Nerves Neurotrophic factors Oils & fats Pollutants Proteins Reporter gene RNA Skin Skin diseases Tryptophan Ultraviolet radiation |
title | Aromatic oil from lavender as an atopic dermatitis suppressant |
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