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2023_DentMat_Immunomodulatory_AparicioC_postprint.pdf (1.24 MB)

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Data de publicació

2023-01-13

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cc by-nc-nd (c) The Academy of Dental Materials, 2023
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/207292

Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing

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Recurs relacionat

https://doi.org/10.1016/j.dental.2023.01.001

Resum

Peri-implantitis, caused by an inflammatory response to pathogens, is the leading cause of dental implant failure. Poor soft tissue healing surrounding implants - caused by inadequate surface properties - leads to infection, inflammation, and dysregulated keratinocyte and macrophage function. One activated inflammatory response, active around peri-implantitis compared to healthy sites, is the IL-23/IL-17A cytokine axis. Implant surfaces can be synthesized with peptide nanocoatings to present immunomodulatory motifs to target peri-implant keratinocytes to control macrophage polarization and regulate inflammatory axises toward enhancing soft tissue healing.We synthesized an IL-23 receptor (IL-23R) noncompetitive antagonist peptide nanocoating using silanization and evaluated keratinocyte secretome changes and macrophage polarization (M1-like "pro-inflammatory" vs. M2-like "pro-regenerative").IL-23R antagonist peptide nanocoatings were successfully synthesized on titanium, to model dental implant surfaces, and compared to nonfunctional nanocoatings and non-coated titanium. IL-23R antagonist nanocoatings significantly decreased keratinocyte IL-23, and downstream IL-17A, expression compared to controls. This peptide noncompetitive antagonistic function was demonstrated under lipopolysaccharide stimulation. Large scale changes in keratinocyte secretome content, toward a pro-regenerative milieu, were observed from keratinocytes cultured on the IL-23R antagonist nanocoatings compared to controls. Conditioned medium collected from keratinocytes cultured on the IL-23R antagonist nanocoatings polarized macrophages toward a M2-like phenotype, based on increased CD163 and CD206 expression and reduced iNOS expression, compared to controls.Our results support development of IL-23R noncompetitive antagonist nanocoatings to reduce the pro-inflammatory IL-23/17A pathway and augment macrophage polarization toward a pro-regenerative phenotype. Immunomodulatory implant surface engineering may promote soft tissue healing and thereby reduce rates of peri-implantitis.Copyright © 2023 Elsevier Inc. All rights reserved.

Matèries

Implants dentals, Interleucines

Matèries (anglès)

Dental implants, Interleukins

Citació

Pizarek, John A;Fischer, Nicholas G;Aparicio, Conrado. Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing. Dental Materials, 2023, 39, 2, 204-216

Col·leccions

Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC))

Citació

PIZAREK, John A., FISCHER, Nicholas G. i APARICIO, Conrado. Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing. Dental Materials. 2023. Vol. 39, núm. 2, pàgs. 204-216. ISSN 0109-5641. [consulta: 8 de maig de 2026]. Disponible a: https://hdl.handle.net/2445/207292

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