Glycated ferritin increases the in vitro expression of TLR2 and TLR4 in peripheral blood CD14+ cells obtained from patients with prediabetes

Jose Manuel Galvan-Moroyoqui, Juan Manuel Martmez-Soto, Luis Fernando Lopez-Soto, Jesus Adriana Soto-Guzman1., Alma Yolanda Camacho-Villa, Gerardo Alvarez-Hernandez, Ana Lourdes Mata-Pineda, Maria del Carmen Candia-Plata*

*Autor correspondiente de este trabajo

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

Resumen

Serum ferritin is a widely-used marker of inflammation in prediabetes, diabetes and atherosclerosis. In these cases, progressive endothelial damage may involve the participation of toll-like receptors (TLR). The aim of this study was to determine the expression of TLR2 and TLR4 in peripheral blood mononuclear cell (PBMC)-derived CD 14+ cells from subjects with prediabetes and with a high level of serum ferritin both at baseline and after in vitro cell stimulation with gly-cated ferritin. Blood samples were drawn from 22 subjects (13 with prediabetes and 9 with normoglycemia). Serum ferritin levels were measured by ELISA, while the expression of TLR2 and TLR4 in PBMC-derived CD 14+ cells was determined by flow cytometry. IL-6 and IL-8 cytokines in PBMC-derived CD 14+ supernatants were measured by ELISA. Subjects with prediabetes had a higher baseline expression of TLR4 in PBMC-derived CD 14+ cells than was observed in cells from normoglycemic subjects (p<0.05). Glycated ferritin increased the expression of both TLR2 and TLR4 as well as IL-6 and IL-8 in PBMC-derived CD 14+ cells from subjects with prediabetes when compared to normoglycemic subjects (p<0.05). We concluded that in prediabetes, the increased basal expression of TLR4 could be part of the low-grade inflammation, which could be increased by glycated ferritin.

Idioma originalInglés
Páginas (desde-hasta)305-312
Número de páginas8
PublicaciónArchives of Biological Sciences
Volumen72
N.º3
DOI
EstadoPublicada - 2020

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© 2020 by the Serbian Biological Society. All rights reserved.

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