Allicin May Promote Reversal of T-Cell Dysfunction in Periodontitis via the PD-1 Pathway
We evaluated the role of allicin in periodontitis using an in silico and in vitro design. An in silico docking analysis was performed to assess the plausible interactions between allicin and . The cytokine profile of gingival crevicular fluid (GCF) samples obtained from periodontitis patients was es...
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Published in: | International journal of molecular sciences Vol. 22; no. 17; p. 9162 |
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Main Authors: | , , , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Switzerland
MDPI AG
25-08-2021
MDPI |
Subjects: | |
Online Access: | Get full text |
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Summary: | We evaluated the role of allicin in periodontitis using an in silico and in vitro design. An in silico docking analysis was performed to assess the plausible interactions between allicin and
. The cytokine profile of gingival crevicular fluid (GCF) samples obtained from periodontitis patients was estimated by cytometric bead array. CD3+ lymphocytes isolated from the peripheral blood were sorted and characterized using immunomagnetic techniques. Cultured and expanded lymphocytes were treated with the GCF samples to induce T-cell exhaustion. Optimum concentrations of allicin were added to exhausted lymphocytes to compare the expression of
and
gene expression at baseline and post-treatment. Allicin was found to bind to the
molecule as revealed by the in-silico experiment, which is possibly an inhibitory interaction although not proven. GCF from periodontitis patients had significantly higher concentrations of TNF-α, CCL2, IL-6, IFN-γ, and CXCL8 than controls. GCF treatment of CD3+ lymphocytes from the periodontitis patients significantly increased expression of T-cell exhaustion markers
and
. Allicin administration with GCF treatment resulted in significant lowering of the expression of exhaustion markers. Allicin may exert an immunostimulatory role and reverse immune-destructive mechanisms such as T-cell exhaustion. |
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ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms22179162 |