Immunological role of prostaglandin E2 production in mouse auditory cells in response to LPS.
The effect of LPS on the production of prostaglandin E2 (PGE2) in mouse HEI-OC1 auditory cells was examined. HEI-OC1 auditory cells constitutively produce a small amount of PGE2. LPS augmented the PGE2 production via enhanced cyclooxygenase 2 (COX2) expression. LPS-induced augmentation of COX2 expression was dependent on up-regulation of COX2 mRNA expression. LPS induced the production of TNF-α, but not IL-1β· An anti-TNF-α neutralizing Ab significantly inhibited PGE2 production and COX2 mRNA expression in response to LPS. LPS-induced PGE2 production was prevented by a series of pharmacological signaling inhibitors to NF-κB and MAPKs. Pam3CSK4 as a TLR2 ligand, as well as LPS as a TLR4 ligand, augmented the PGE2 production. However, poly I:C as a TLR3 ligand, imiquimod as a TLR7 ligand and CpG DNA as a TLR9 ligand did not augment it. HEI-OC1 cells expressed TLR2, TLR4 and TLR9, but not TLR3 or TLR7. The putative role of LPS-induced PGE2 production in auditory cells is discussed.
Department of Otolaryngology, Aichi Medical University School of Medicine, Aichi, Japan.
Tohru
T
Tanigawa
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan.
Erdenezaya
E
Odkhuu
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan.
Akiko
A
Morikawa
Shinkawa Clinic, Kanagawa, Japan.
Ken
K
Hayashi
Department of Otolaryngology, Aichi Gakuin University, Aichi, Japan.
Takashi
T
Sato
Department of Cardiology, Graduate School of Medical Sciences, Nagoya University, Aichi, Japan.
Rei
R
Shibata
Department of Otolaryngology, National Hospital Organization Tokyo Medical Center, Tokyo, Japan.
Fumiyuki
F
Goto
Department of Otolaryngology, Aichi Medical University School of Medicine, Aichi, Japan.
Hiromi
H
Ueda
Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Aichi, Japan yokochi@aichi-med-u.ac.jp.
Takashi
T
Yokochi
D000818:Animals; D002460:Cell Line; D003051:Cochlea / Q000166:cytology / Q000276:immunology*; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D015232:Dinoprostone / Q000276:immunology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis; D051217:Toll-Like Receptor 9 / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D015854:Up-Regulation / Q000187:drug effects
C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; C493486:Tlr2 protein, mouse; C493487:Tlr4 protein, mouse; C495370:Tlr9 protein, mouse; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4; D051217:Toll-Like Receptor 9; D014409:Tumor Necrosis Factor-alpha; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D020928:Mitogen-Activated Protein Kinases; D015232:Dinoprostone
Auditory cells; HEI-OC1 cells; cyclooxygenase; lipopolysaccharide; prostaglandin E2