TY - JOUR
T1 - Priming of human oral epithelial cells by interferon-γ to secrete cytokines in response to lipopolysaccharides, lipoteichoic acids and peptidoglycans
AU - Uehara, A.
AU - Sugawara, S.
AU - Takada, H.
PY - 2002
Y1 - 2002
N2 - An earlier study reported that human gingival epithelial cells in primary culture and oral epithelial cell lines KB and HSC-2 cells were devoid of membrane CD14 (mCD14) and did not show enhanced production of interleukin (IL)-8 or granulocyte macrophage-colony stimulating factor (GM-CSF) upon stimulation with bacterial cell-surface components such as lipopolysaccharide (LPS), lipoteichoic acid (LTA), peptidoglycan (PGN) and synthetic muramyldipeptide (MDP) even in the presence of serum. The present study demonstrated that after treatment with interferon (IFN)-γ for 3 days, these cells secreted IL-8 and GM-CSF in response to the bacterial components. Treatment with IFN-γ enhanced Toll-like receptor (TLR) 2, TLR4, MD-2 and MyD88 mRNA expression as determined by reverse transcriptase PCR. Anti-TLR2 and anti-TLR4 monoclonal antibodies (MAbs) inhibited the IL-8 production induced by PGN and LTA as well as LPS, respectively, in IFN-γ-primed oral epithelial cells, whereas neither MAb inhibited IL-8 production induced by MDP. These findings suggested that IFN-γ primed oral epithelial cells to produce cytokines upon stimulation with various bacterial components by up-regulation of the TLR system.
AB - An earlier study reported that human gingival epithelial cells in primary culture and oral epithelial cell lines KB and HSC-2 cells were devoid of membrane CD14 (mCD14) and did not show enhanced production of interleukin (IL)-8 or granulocyte macrophage-colony stimulating factor (GM-CSF) upon stimulation with bacterial cell-surface components such as lipopolysaccharide (LPS), lipoteichoic acid (LTA), peptidoglycan (PGN) and synthetic muramyldipeptide (MDP) even in the presence of serum. The present study demonstrated that after treatment with interferon (IFN)-γ for 3 days, these cells secreted IL-8 and GM-CSF in response to the bacterial components. Treatment with IFN-γ enhanced Toll-like receptor (TLR) 2, TLR4, MD-2 and MyD88 mRNA expression as determined by reverse transcriptase PCR. Anti-TLR2 and anti-TLR4 monoclonal antibodies (MAbs) inhibited the IL-8 production induced by PGN and LTA as well as LPS, respectively, in IFN-γ-primed oral epithelial cells, whereas neither MAb inhibited IL-8 production induced by MDP. These findings suggested that IFN-γ primed oral epithelial cells to produce cytokines upon stimulation with various bacterial components by up-regulation of the TLR system.
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U2 - 10.1099/0022-1317-51-8-626
DO - 10.1099/0022-1317-51-8-626
M3 - Article
C2 - 12171292
AN - SCOPUS:0036073782
SN - 0022-2615
VL - 51
SP - 626
EP - 634
JO - Journal of Medical Microbiology
JF - Journal of Medical Microbiology
IS - 8
ER -