Mannan Oligosaccharide Could Attenuate Ochratoxin A-Induced Immunosuppression with Long-Time Exposure Instead of Immunostimulation with Short-Time Exposure

甘露聚糖 赭曲霉毒素A 免疫抑制 自噬 毒性 化学 磷酸化 药理学 真菌毒素 免疫系统 生物 免疫学 细胞生物学 细胞凋亡 生物化学 多糖 有机化学 植物
作者
Wenmiao He,Jiarui Su,Dandan Liu,Kehe Huang
出处
期刊:Journal of Agricultural and Food Chemistry [American Chemical Society]
卷期号:69 (38): 11461-11469 被引量:8
标识
DOI:10.1021/acs.jafc.1c04485
摘要

Our previous study showed that ochratoxin A (OTA), one of the most common mycotoxins in feed, could induce immunosuppression with long-time exposure but immunostimulation with short-time exposure. However, limited studies for the control of OTA-induced two-way immune toxicity were carried out. This study explored the effects of mannan oligosaccharide (MOS), a glucomannoprotein complex with immunoregulatory capability derived from the yeast cell wall, on OTA-induced immune toxicity and its underlying mechanisms. Surprisingly, the results showed that MOS significantly attenuated immunosuppression induced by long-time OTA treatment but did not provide protection against immunostimulation induced by short-time OTA treatment on porcine alveolar macrophages (PAMs), as demonstrated by the expressions of inflammatory cytokines and the capability of migration and phagocytosis. Further, MOS increased the OTA-inhibited autophagy level and the JNK phosphorylation level on PAMs with long-time OTA treatment. In addition, the inhibition of autophagy by 3-MA or the inhibition of JNK phosphorylation by SP600125 could partly block the protective effects of MOS on OTA-induced immunosuppression. Importantly, the inhibition of JNK phosphorylation down-regulated the MOS-promoted autophagy level. In conclusion, MOS could attenuate OTA-induced immunosuppression with short-time exposure on PAMs through activating JNK-mediated autophagy but had no significant effects on OTA-induced immunostimulation with short-time exposure. Our study provides new insights into the application of MOS as an immunoregulator against mycotoxin-induced immune toxicity.
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