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Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles
OBJECTIVE: Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a member of the carcinoembryonic antigen family. Although its expression has been found in chronic oral inflammatory epithelium, this study aimed to know whether CEACAM1 in oral keratinocytes participates in host immun...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Faculdade De Odontologia De Bauru - USP
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9651918/ https://www.ncbi.nlm.nih.gov/pubmed/36350873 http://dx.doi.org/10.1590/1678-7757-2022-0158 |
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author | SAKUMA, Miyuki OHTA, Kouji FUKADA, Shohei AKAGI, Misaki KATO, Hiroki ISHIDA, Yoko NARUSE, Takako TAKECHI, Masaaki SHIGEISHI, Hideo NISHI, Hiromi AIKAWA, Tomonao |
author_facet | SAKUMA, Miyuki OHTA, Kouji FUKADA, Shohei AKAGI, Misaki KATO, Hiroki ISHIDA, Yoko NARUSE, Takako TAKECHI, Masaaki SHIGEISHI, Hideo NISHI, Hiromi AIKAWA, Tomonao |
author_sort | SAKUMA, Miyuki |
collection | PubMed |
description | OBJECTIVE: Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a member of the carcinoembryonic antigen family. Although its expression has been found in chronic oral inflammatory epithelium, this study aimed to know whether CEACAM1 in oral keratinocytes participates in host immune response against Candida albicans . METHODOLOGY: We investigated CEACAM1 expression in oral keratinocytes induced by C. albicans as well as by Candida cell wall component β-glucan particles (β-GPs). Furthermore, the effects of CEACAM1 on β-GPs-induced heme oxygenase-1 (HO-1) expression and its related signals were examined. RESULTS: Fluorescence staining showed CEACAM1 expression in oral keratinocytes (RT7) cells, whereas quantitative reverse transcription (RT)-PCR indicated that both live and heat-killed C. albicans increased CEACAM1 mRNA expression in RT7 cells. Examinations using quantitative RT-PCR and western blotting indicated that CEACAM1 expression was also increased by β-GPs derived from C. albicans . Specific siRNA for CEACAM1 decreased HO-1 expression induced by β-GPs from C. albicans as well as the budding yeast microorganism Saccharomyces cerevisiae . Moreover, knockdown of CEACAM1 decreased β-GPs-induced ROS activity in the early phase and translocation of Nrf2 into the nucleus. CONCLUSION: CEACAM1 in oral keratinocytes may have a critical role in regulation of HO-1 for host immune defense during Candida infection. |
format | Online Article Text |
id | pubmed-9651918 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Faculdade De Odontologia De Bauru - USP |
record_format | MEDLINE/PubMed |
spelling | pubmed-96519182022-11-14 Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles SAKUMA, Miyuki OHTA, Kouji FUKADA, Shohei AKAGI, Misaki KATO, Hiroki ISHIDA, Yoko NARUSE, Takako TAKECHI, Masaaki SHIGEISHI, Hideo NISHI, Hiromi AIKAWA, Tomonao J Appl Oral Sci Original Article OBJECTIVE: Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is a member of the carcinoembryonic antigen family. Although its expression has been found in chronic oral inflammatory epithelium, this study aimed to know whether CEACAM1 in oral keratinocytes participates in host immune response against Candida albicans . METHODOLOGY: We investigated CEACAM1 expression in oral keratinocytes induced by C. albicans as well as by Candida cell wall component β-glucan particles (β-GPs). Furthermore, the effects of CEACAM1 on β-GPs-induced heme oxygenase-1 (HO-1) expression and its related signals were examined. RESULTS: Fluorescence staining showed CEACAM1 expression in oral keratinocytes (RT7) cells, whereas quantitative reverse transcription (RT)-PCR indicated that both live and heat-killed C. albicans increased CEACAM1 mRNA expression in RT7 cells. Examinations using quantitative RT-PCR and western blotting indicated that CEACAM1 expression was also increased by β-GPs derived from C. albicans . Specific siRNA for CEACAM1 decreased HO-1 expression induced by β-GPs from C. albicans as well as the budding yeast microorganism Saccharomyces cerevisiae . Moreover, knockdown of CEACAM1 decreased β-GPs-induced ROS activity in the early phase and translocation of Nrf2 into the nucleus. CONCLUSION: CEACAM1 in oral keratinocytes may have a critical role in regulation of HO-1 for host immune defense during Candida infection. Faculdade De Odontologia De Bauru - USP 2022-11-04 /pmc/articles/PMC9651918/ /pubmed/36350873 http://dx.doi.org/10.1590/1678-7757-2022-0158 Text en https://creativecommons.org/licenses/by/4.0/ 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 work is properly cited. |
spellingShingle | Original Article SAKUMA, Miyuki OHTA, Kouji FUKADA, Shohei AKAGI, Misaki KATO, Hiroki ISHIDA, Yoko NARUSE, Takako TAKECHI, Masaaki SHIGEISHI, Hideo NISHI, Hiromi AIKAWA, Tomonao Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles |
title | Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles |
title_full | Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles |
title_fullStr | Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles |
title_full_unstemmed | Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles |
title_short | Effects of CEACAM1 in oral keratinocytes on HO-1 expression induced by Candida β-glucan particles |
title_sort | effects of ceacam1 in oral keratinocytes on ho-1 expression induced by candida β-glucan particles |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9651918/ https://www.ncbi.nlm.nih.gov/pubmed/36350873 http://dx.doi.org/10.1590/1678-7757-2022-0158 |
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