Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i>
Oral mucositis, inflammation, and ulceration that occur in the oral cavity can manifest in significant pain. A formulation was designed to investigate the potential of vitamin E to ameliorate inflammation resulting from <i>Candida albicans</i> in cell-based systems. Human gingival fibrob...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2020-05-01
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| Series: | Microorganisms |
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| Online Access: | https://www.mdpi.com/2076-2607/8/6/804 |
| _version_ | 1797566980568383488 |
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| author | Silvana Barros Ana Paula D. Ribeiro Steven Offenbacher Zvi G. Loewy |
| author_facet | Silvana Barros Ana Paula D. Ribeiro Steven Offenbacher Zvi G. Loewy |
| author_sort | Silvana Barros |
| collection | DOAJ |
| description | Oral mucositis, inflammation, and ulceration that occur in the oral cavity can manifest in significant pain. A formulation was designed to investigate the potential of vitamin E to ameliorate inflammation resulting from <i>Candida albicans</i> in cell-based systems. Human gingival fibroblasts and THP1 cells were stimulated with heat killed <i>C. albicans</i> and <i>Porphyromonas gingivalis</i> LPS (agonists). Unstimulated cells were included as controls. Cells were also simultaneously treated with a novel denture adhesive formulation that contains vitamin E (antagonist). The experimental conditions included cells exposed to the experimental formulation or the vehicle for 2 h for mRNA extraction and analysis, and cells left for 24 h under those experimental conditions for analysis of protein expression by ELISA. ssAffymetrix expression microarray pathway analyses demonstrated that the tested formulation exhibited a statistically significant (<i>p</i> < 0.05) inhibition of the following key inflammatory pathways: TLR 6, IL-1 signaling (IRAK, A20), NF-kappaB, IL-6 signaling (gp130, JK2 and GRB2), TNF signaling (TNF receptor) and Arachidonic acid metabolism (PLA2). Quantitative PCR array analysis confirmed the downregulation of key inflammatory genes when cells under adhesive treatment were challenged with heat killed <i>C. albicans</i>. PGE2 secretion was inhibited by the tested formulation only on THP1 cells after 24 h stimulation with <i>C. albicans</i>. These results suggest that the active formulation containing vitamin E acetate can modulate inflammatory responses, through anti-inflammatory actions as indicated by in vitro experimental conditions. |
| first_indexed | 2024-03-10T19:35:09Z |
| format | Article |
| id | doaj.art-e2730e82b34845e5bcb66639b91082c1 |
| institution | Directory Open Access Journal |
| issn | 2076-2607 |
| language | English |
| last_indexed | 2024-03-10T19:35:09Z |
| publishDate | 2020-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Microorganisms |
| spelling | doaj.art-e2730e82b34845e5bcb66639b91082c12023-11-20T01:50:38ZengMDPI AGMicroorganisms2076-26072020-05-018680410.3390/microorganisms8060804Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i>Silvana Barros0Ana Paula D. Ribeiro1Steven Offenbacher2Zvi G. Loewy3Department of Periodontology, School of Dentistry, University of North Carolina, Chapel Hill, NC 27599, USADepartment of Restorative Dental Sciences, College of Dentistry, University of Florida, Gainesville, FL 32610, USADepartment of Periodontology, School of Dentistry, University of North Carolina, Chapel Hill, NC 27599, USADepartment of Pharmaceutical and Biomedical Sciences, Touro College of Pharmacy, New York, NY 10027, USAOral mucositis, inflammation, and ulceration that occur in the oral cavity can manifest in significant pain. A formulation was designed to investigate the potential of vitamin E to ameliorate inflammation resulting from <i>Candida albicans</i> in cell-based systems. Human gingival fibroblasts and THP1 cells were stimulated with heat killed <i>C. albicans</i> and <i>Porphyromonas gingivalis</i> LPS (agonists). Unstimulated cells were included as controls. Cells were also simultaneously treated with a novel denture adhesive formulation that contains vitamin E (antagonist). The experimental conditions included cells exposed to the experimental formulation or the vehicle for 2 h for mRNA extraction and analysis, and cells left for 24 h under those experimental conditions for analysis of protein expression by ELISA. ssAffymetrix expression microarray pathway analyses demonstrated that the tested formulation exhibited a statistically significant (<i>p</i> < 0.05) inhibition of the following key inflammatory pathways: TLR 6, IL-1 signaling (IRAK, A20), NF-kappaB, IL-6 signaling (gp130, JK2 and GRB2), TNF signaling (TNF receptor) and Arachidonic acid metabolism (PLA2). Quantitative PCR array analysis confirmed the downregulation of key inflammatory genes when cells under adhesive treatment were challenged with heat killed <i>C. albicans</i>. PGE2 secretion was inhibited by the tested formulation only on THP1 cells after 24 h stimulation with <i>C. albicans</i>. These results suggest that the active formulation containing vitamin E acetate can modulate inflammatory responses, through anti-inflammatory actions as indicated by in vitro experimental conditions.https://www.mdpi.com/2076-2607/8/6/804in vitrocandidiasisagonist |
| spellingShingle | Silvana Barros Ana Paula D. Ribeiro Steven Offenbacher Zvi G. Loewy Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i> Microorganisms in vitro candidiasis agonist |
| title | Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i> |
| title_full | Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i> |
| title_fullStr | Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i> |
| title_full_unstemmed | Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i> |
| title_short | Anti-Inflammatory Effects of Vitamin E in Response to <i>Candida albicans</i> |
| title_sort | anti inflammatory effects of vitamin e in response to i candida albicans i |
| topic | in vitro candidiasis agonist |
| url | https://www.mdpi.com/2076-2607/8/6/804 |
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