2026-04-13T13:15:10Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/2072922025-11-19T10:45:39Zcom_2072_1057col_2072_478902col_2072_478917

Immunomodulatory IL-23 receptor antagonist peptide nanocoatings for implant soft tissue healing Pizarek, John A. Fischer, Nicholas G. Aparicio, Conrado Implants dentals Interleucines Dental implants Interleukins 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. 2024-02-07T19:34:20Z 2024-02-07T19:34:20Z 2023-01-13 2024-01-31T10:56:29Z info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion https://doi.org/10.1016/j.dental.2023.01.001 Dental Materials, 2023, vol. 39, num. 2, p. 204-216 https://doi.org/10.1016/j.dental.2023.01.001 cc by-nc-nd (c) The Academy of Dental Materials, 2023 http://creativecommons.org/licenses/by-nc-nd/3.0/es/ info:eu-repo/semantics/openAccess Elsevier B. V. Articles publicats en revistes (Institut de Bioenginyeria de Catalunya (IBEC))