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Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome

While cigarette smoke compounds are known to have immunosuppressive effects on the oral mucosa, the relationship between in vivo immune dysfunction caused by smoking and the development of oral Candida infections remains largely unexplored. In a recent issue of The Journal of Cellular and Molecular...

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Detalles Bibliográficos
Autores principales: Osman, Marwan, Papon, Nicolas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8500950/
https://www.ncbi.nlm.nih.gov/pubmed/34486221
http://dx.doi.org/10.1111/jcmm.16901
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author Osman, Marwan
Papon, Nicolas
author_facet Osman, Marwan
Papon, Nicolas
author_sort Osman, Marwan
collection PubMed
description While cigarette smoke compounds are known to have immunosuppressive effects on the oral mucosa, the relationship between in vivo immune dysfunction caused by smoking and the development of oral Candida infections remains largely unexplored. In a recent issue of The Journal of Cellular and Molecular Medicine, Ye and colleagues provide evidence that smoking increases oral mucosa susceptibility to Candida albicans infection via the activation of the Nrf2 pathway, which in turn negatively regulates the NLRP3 inflammasome. This opens new perspective in considering Nrf2 as a relevant target for smoking‐induced C. albicans‐related oral diseases.
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spelling pubmed-85009502021-10-12 Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome Osman, Marwan Papon, Nicolas J Cell Mol Med Commentary While cigarette smoke compounds are known to have immunosuppressive effects on the oral mucosa, the relationship between in vivo immune dysfunction caused by smoking and the development of oral Candida infections remains largely unexplored. In a recent issue of The Journal of Cellular and Molecular Medicine, Ye and colleagues provide evidence that smoking increases oral mucosa susceptibility to Candida albicans infection via the activation of the Nrf2 pathway, which in turn negatively regulates the NLRP3 inflammasome. This opens new perspective in considering Nrf2 as a relevant target for smoking‐induced C. albicans‐related oral diseases. John Wiley and Sons Inc. 2021-09-05 2021-10 /pmc/articles/PMC8500950/ /pubmed/34486221 http://dx.doi.org/10.1111/jcmm.16901 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Commentary
Osman, Marwan
Papon, Nicolas
Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome
title Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome
title_full Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome
title_fullStr Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome
title_full_unstemmed Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome
title_short Smoking‐aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome
title_sort smoking‐aggravated oral candidiasis: nrf2 pathway dampens nlrp3 inflammasome
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8500950/
https://www.ncbi.nlm.nih.gov/pubmed/34486221
http://dx.doi.org/10.1111/jcmm.16901
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