Inhibition of cytokine and surface antigen expression in LPS-stimulated murine macrophages by triethylene glycol dimethacrylate.
Dental resin monomers like triethylene glycol dimethacrylate (TEGDMA) cause a shift in the cellular redox balance which influences redox-sensitive signaling pathways. The immediate response of the innate immune system to inflammatory challenges is controlled by related pathways. Therefore, the influence of TEGDMA on the expression of the pro- and anti-inflammatory cytokines TNF-alpha, IL-6, and IL-10 and surface antigens (CD14, CD40, CD80, CD86, CD54, MHC class I and II) was analyzed in RAW264.7 macrophages. No significant change in cytokine production or surface antigen expression was detected after the macrophages were treated with increasing TEGDMA concentrations for 6, 24, and 48h. However, co-stimulation with the bacterial endotoxin lipopolysaccharide (LPS) and TEGDMA resulted in a concentration-dependent inhibition of LPS-induced release of TNF-alpha, IL-6, and IL-10 by about 90% as detected by ELISA. Flow-cytometric analyses indicated an LPS-stimulated expression of all surface antigens. The LPS-induced expression of CD14 was inhibited by high TEGDMA concentrations. CD40 and CD80 expressions were down-regulated by TEGDMA in LPS-stimulated cells, and CD86 as well as MHC class I expression was inhibited to a lesser extent. The LPS-stimulated expression of CD54 (ICAM-1) was increased about twofold by increasing TEGDMA concentrations after a 24 and 48h exposure. Thus, the ability of macrophages to induce an appropriate immune response is inhibited by TEGDMA which reduces cytokine production and expression of surface antigens.
Eckhardt
Alexander
A
Department of Operative Dentistry and Periodontology, University of Regensburg, Germany.
Harorli
Tolga
T
Limtanyakul
Jirakant
J
Hiller
Karl-Anton
KA
Bosl
Claudia
C
Bolay
Carola
C
Reichl
Franz-Xaver
FX
Schmalz
Gottfried
G
Schweikl
Helmut
H
D000818:Animals; D000954:Antigens, Surface / Q000378:metabolism*; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008264:Macrophages / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D051379:Mice; D011092:Polyethylene Glycols / Q000494:pharmacology*; D011109:Polymethacrylic Acids / Q000494:pharmacology*
D000954:Antigens, Surface; D016207:Cytokines; D008070:Lipopolysaccharides; D011109:Polymethacrylic Acids; C020946:triethylene glycol dimethacrylate; D011092:Polyethylene Glycols