Streptococcus anginosus由来抗原によるマウス腹腔滲出細胞からのNO産生誘導機構
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概要
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Nitric oxide (NO) has been implicated in macrophage-mediated cytotoxicity against various pathogens and may play a role in persistent or latent infections. However, its overproduction induced by some bacterial antigens could cause damage to host tissues and cellular DNA. We have previously reported a novel bioactive antigen (SAA) from a culture supernatant of Streptococcus anginosus that induces NO synthesis by murine peritoneal exudate cells (PEC). In this study, I performed a further assessment of SAA-induced NO synthesis by PEC. The results indicated that SAA stimulated the macrophages in PEC as well as a murine macrophage cell line, J774.1, to produce NO with the accumulation of inducible NO synthase (iNOS) mRNA. SAA also stimulated the non-macrophage cells in PEC to produce IFN- γ, however, the endogenous IFN-γ was not involved in the SAA-induced NO synthesis and iNOS mRNA accumulation by the macrophages. Further, phosphorylation of both p38 and ERK1/2 mitogen-activated protein (MAP) kinase was observed in macrophages by the stimulation with SAA but p38 MAP kinase pathway could solely correlate with SAA-induced NO synthesis. Thus, the present results suggest that S. anginosus, by a bioactive antigen, SAA, could stimulate macrophages through p38 MAP kinase nathwav to induce NO svnthesis without heln of the endogenous TFN-γ.
- 岩手医科大学歯学会の論文
- 2004-04-26
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