Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes

Abstract Carbon dioxide (CO2) is the predominant gas molecule emitted during aerobic respiration. Although CO2 can improve blood circulation in the skin via its vasodilatory effects, its effects on skin inflammation remain unclear. The present study aimed to examine the anti-inflammatory effects of...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Keimon Sayama, Katsuyuki Yuki, Keiichi Sugata, Satoko Fukagawa, Tetsuji Yamamoto, Shigaku Ikeda, Takatoshi Murase
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a12a9e5bf85d4525b233ffafb69adc78
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:a12a9e5bf85d4525b233ffafb69adc78
record_format	dspace
spelling	oai:doaj.org-article:a12a9e5bf85d4525b233ffafb69adc782021-12-02T14:01:24ZCarbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes10.1038/s41598-020-79519-02045-2322https://doaj.org/article/a12a9e5bf85d4525b233ffafb69adc782021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-79519-0https://doaj.org/toc/2045-2322Abstract Carbon dioxide (CO2) is the predominant gas molecule emitted during aerobic respiration. Although CO2 can improve blood circulation in the skin via its vasodilatory effects, its effects on skin inflammation remain unclear. The present study aimed to examine the anti-inflammatory effects of CO2 in human keratinocytes and skin. Keratinocytes were cultured under 15% CO2, irradiated with ultraviolet B (UVB), and their inflammatory cytokine production was analyzed. Using multiphoton laser microscopy, the effect of CO2 on pH was observed by loading a three-dimensional (3D)-cultured epidermis with a high-CO2 concentration formulation. Finally, the effect of CO2 on UVB-induced erythema was confirmed. CO2 suppressed the UVB-induced production of tumor necrosis factor-α (TNFα) and interleukin-6 (IL-6) in keratinocytes and the 3D epidermis. Correcting medium acidification with NaOH inhibited the CO2-induced suppression of TNFα and IL-6 expression in keratinocytes. Moreover, the knockdown of H+-sensing G protein-coupled receptor 65 inhibited the CO2-induced suppression of inflammatory cytokine expression and NF-κB activation and reduced CO2-induced cyclic adenosine monophosphate production. Furthermore, the high-CO2 concentration formulation suppressed UVB-induced erythema in human skin. Hence, CO2 suppresses skin inflammation and can be employed as a potential therapeutic agent in restoring skin immune homeostasis.Keimon SayamaKatsuyuki YukiKeiichi SugataSatoko FukagawaTetsuji YamamotoShigaku IkedaTakatoshi MuraseNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-10 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Keimon Sayama Katsuyuki Yuki Keiichi Sugata Satoko Fukagawa Tetsuji Yamamoto Shigaku Ikeda Takatoshi Murase Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes
description	Abstract Carbon dioxide (CO2) is the predominant gas molecule emitted during aerobic respiration. Although CO2 can improve blood circulation in the skin via its vasodilatory effects, its effects on skin inflammation remain unclear. The present study aimed to examine the anti-inflammatory effects of CO2 in human keratinocytes and skin. Keratinocytes were cultured under 15% CO2, irradiated with ultraviolet B (UVB), and their inflammatory cytokine production was analyzed. Using multiphoton laser microscopy, the effect of CO2 on pH was observed by loading a three-dimensional (3D)-cultured epidermis with a high-CO2 concentration formulation. Finally, the effect of CO2 on UVB-induced erythema was confirmed. CO2 suppressed the UVB-induced production of tumor necrosis factor-α (TNFα) and interleukin-6 (IL-6) in keratinocytes and the 3D epidermis. Correcting medium acidification with NaOH inhibited the CO2-induced suppression of TNFα and IL-6 expression in keratinocytes. Moreover, the knockdown of H+-sensing G protein-coupled receptor 65 inhibited the CO2-induced suppression of inflammatory cytokine expression and NF-κB activation and reduced CO2-induced cyclic adenosine monophosphate production. Furthermore, the high-CO2 concentration formulation suppressed UVB-induced erythema in human skin. Hence, CO2 suppresses skin inflammation and can be employed as a potential therapeutic agent in restoring skin immune homeostasis.
format	article
author	Keimon Sayama Katsuyuki Yuki Keiichi Sugata Satoko Fukagawa Tetsuji Yamamoto Shigaku Ikeda Takatoshi Murase
author_facet	Keimon Sayama Katsuyuki Yuki Keiichi Sugata Satoko Fukagawa Tetsuji Yamamoto Shigaku Ikeda Takatoshi Murase
author_sort	Keimon Sayama
title	Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes
title_short	Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes
title_full	Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes
title_fullStr	Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes
title_full_unstemmed	Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes
title_sort	carbon dioxide inhibits uvb-induced inflammatory response by activating the proton-sensing receptor, gpr65, in human keratinocytes
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/a12a9e5bf85d4525b233ffafb69adc78
work_keys_str_mv	AT keimonsayama carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes AT katsuyukiyuki carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes AT keiichisugata carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes AT satokofukagawa carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes AT tetsujiyamamoto carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes AT shigakuikeda carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes AT takatoshimurase carbondioxideinhibitsuvbinducedinflammatoryresponsebyactivatingtheprotonsensingreceptorgpr65inhumankeratinocytes
_version_	1718392159235735552

Carbon dioxide inhibits UVB-induced inflammatory response by activating the proton-sensing receptor, GPR65, in human keratinocytes

Ejemplares similares