HEMA-induced oxidative stress inhibits NF-κB nuclear translocation and TNF release from LTA- and LPS-stimulated immunocompetent cells

Objective: The release of inflammatory cytokines from antigen-stimulated cells of the Resin monomer immune system is inhibited by resin monomers such as 2-hydroxyethyl methacrylate HEMA (HEMA). Although the formation of oxidative stress in cells exposed to HEMA is firmly estab- Oxidative stress lished, the mechanism behind the inhibited cytokine secretion is only partly known. The Cytokine present investigation presents evidence regarding the role of HEMA-induced oxidative stress NF-KB in the secretion of the pro-inflammatory cytokine TNFoL from cells exposed to the antigens Nrf2 LTA (lipoteichoic acid) or LPS (lipopolysaccharide) of cariogenic microorganisms using BSO (L-buthionine sulfoximine) or NAC (N-acetyl cysteine) to inhibit or stabilize the amounts of the antioxidant glutathione. Method: RAW264.7 mouse macrophages were treated with LTA, LPS or HEMA in the presence of BSO or NAC for 1h or 24h. Secretion of TNFoL from cell cultures was analyzed by ELISA, and the formation of reactive oxygen (ROS) or nitrogen species (RNS) was determined by flow cytometry. Protein expression was detected by Western blotting. Results: The release of TNF alpha in both LTA- and LPS-exposed cells was decreased by HEMA, and this concentration-dependent inhibitory effect was amplified by BSO or NAC. LTA- and LPS-stimulated expression of the redox-sensitive transcription factor NF-alpha B (p65) in cell nuclei decreased in the presence of HEMA because the translocation of p65 from the cytosol was prevented by oxidative stress specifically increased by the monomer. Conclusions: A disturbance of the cellular redox balance, particularly induced by HEMA, is a crucial factor in the inhibition of LTA- and LPS-stimulated signalling pathways leading to TNF alpha secretion. (C) 2020 The Academy of Dental Materials. Published by Elsevier Inc. All rights reserved.