Division of Genetics and Mutagenesis, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo, 158-8501, Japan,
Mycotoxin Res. 2013 Nov;29(4):229-34. doi: 10.1007/s12550-013-0175-x. Epub 2013 Jul 30.
The present study evaluated the immunotoxicity of citrinin (CIT), a mycotoxin produced by several Aspergillus, Penicillium, and Monascus species. Because nitric oxide (NO), a pro-inflammatory mediator, plays an important role in the protection from pathogens, we addressed the effect of CIT on NO production by a mouse macrophage-like cell line RAW264 activated with lipopolysaccharide (LPS). LPS-induced NO release from RAW264 cells was inhibited by CIT. Moreover, the transcription and expression of inducible NO synthase (iNOS) by LPS was suppressed by CIT. These results show that CIT suppressed the LPS-induced NO production and iNOS expression, which contribute to the host protection against invading pathogens. This suggests that CIT on LPS-induced NO release may exert adverse effects in macrophages, indicating immunotoxic effects of this toxin. .
本研究评估了桔霉素（CIT）的免疫毒性，CIT 是由几种曲霉属、青霉属和红曲属产生的一种真菌毒素。由于一氧化氮（NO）作为一种促炎介质，在抵御病原体方面发挥着重要作用，我们研究了 CIT 对脂多糖（LPS）激活的小鼠巨噬细胞样细胞系 RAW264 产生 NO 的影响。CIT 抑制 LPS 诱导的 RAW264 细胞中 NO 的释放。此外，CIT 抑制 LPS 诱导的诱导型一氧化氮合酶（iNOS）的转录和表达。这些结果表明，CIT 抑制了 LPS 诱导的 NO 产生和 iNOS 表达，这有助于宿主抵抗入侵的病原体。这表明 CIT 可能对 LPS 诱导的 NO 释放产生不利影响，表明这种毒素具有免疫毒性作用。
