Auditory cells produce nitric oxide in response to bacterial lipopolysaccharide

• Published in: Innate immunity (London, England) England), 2013-04, Vol.19 (2), p.115-120
• Main Authors: Tanigawa, Tohru, Morikawa, Akiko, Hayashi, Ken, Dan, Katsuaki, Tsuchihashi, Nana, Goto, Fumiyuki, Ueda, Hiromi, Yokochi, Takashi
• Format: Article
• Language: English
• Subjects: Animals; Bacteria; Cell Line, Transformed; Cell Survival; Dose-Response Relationship, Immunologic; Hair Cells, Auditory - immunology; Immunity, Innate; Interferon-beta - metabolism; Lipopolysaccharide Receptors - metabolism; Lipopolysaccharides - immunology; Mice; Myeloid Differentiation Factor 88 - metabolism; Nitric Oxide - immunology; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; Signal Transduction - immunology; Toll-Like Receptor 4 - metabolism
• ISSN: 1753-4259; 1753-4267
• DOI: 10.1177/1753425912450347

The NO productivity of auditory cells in response to LPS was examined by using conditionally immortalized murine HEI-OC1 auditory cells. HEI-OC1 cells produced NO in response to LPS ranging from 0.1 µg/ml to 100 µg/ml in a concentration-dependent manner. LPS at 100 µg/ml exhibited no cytotoxic action against HEI-OC1 cells and led to the highest level of NO production. The NO output in LPS-treated HEI-OC1 cells gradually increased up to 72 h. LPS-induced NO production was mediated by the expression of an inducible NO synthase (iNOS) protein. TLR4 and CD14 was expressed on the cell surface of HEI-OC1 cells. LPS augmented the production of IFN-β in the MyD88-independent pathway of LPS signalling. HEI-OC1 cells produced NO in response to a TLR2 ligand but not TLR3 ligand. LPS was suggested to lead to NO production in auditory cells via iNOS expression. The immunological significance of NO production in auditory cells is discussed.