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J Agric Food Chem. 2018 Dec 26. doi: 10.1021/acs.jafc.8b05829. [Epub ahead of print]
Mannan oligosaccharide protects against the AFB1-promoted influenza replication and tissue damages in a TLR4-dependent manner.
Sun Y, Su J, Yang S, Liu Z, Liu D, Gan F, Chen X, Huang K.
Abstract
Our previous study reported that aflatoxin B1 (AFB1) promoted influenza replication. Mannan oligosaccharide (MOS), derived from the cell walls of yeast, is a potent immune-modulator. Here, we investigated the role of MOS in AFB1-promoted influenza replication and further explored the underlying mechanisms. In vitro and in vivo, the exposure to AFB1 alone resulted in significantly decreased weight gain and increased viral replication, as well as lung and spleen damages. Increased influenza replication coupled with increases in TLR4, phosphorylated NF-κB and TNF-α levels. However, MOS given in conjunction with exposure to AFB1 reversed significantly these above changes. Further study indicated that MOS activity was abolished by TLR4 knockout or TLR4 overexpression. Surprisingly, TNF-α played no role in the MOS-mediated protective effects. Collectively, our data suggest that MOS alleviates the AFB1-promoted influenza replication, inflammation and tissue damages in a TLR4-dependent manner.
PMID: 30586993 DOI: 10.1021/acs.jafc.8b05829
Mannan oligosaccharide protects against the AFB1-promoted influenza replication and tissue damages in a TLR4-dependent manner.
Sun Y, Su J, Yang S, Liu Z, Liu D, Gan F, Chen X, Huang K.
Abstract
Our previous study reported that aflatoxin B1 (AFB1) promoted influenza replication. Mannan oligosaccharide (MOS), derived from the cell walls of yeast, is a potent immune-modulator. Here, we investigated the role of MOS in AFB1-promoted influenza replication and further explored the underlying mechanisms. In vitro and in vivo, the exposure to AFB1 alone resulted in significantly decreased weight gain and increased viral replication, as well as lung and spleen damages. Increased influenza replication coupled with increases in TLR4, phosphorylated NF-κB and TNF-α levels. However, MOS given in conjunction with exposure to AFB1 reversed significantly these above changes. Further study indicated that MOS activity was abolished by TLR4 knockout or TLR4 overexpression. Surprisingly, TNF-α played no role in the MOS-mediated protective effects. Collectively, our data suggest that MOS alleviates the AFB1-promoted influenza replication, inflammation and tissue damages in a TLR4-dependent manner.
PMID: 30586993 DOI: 10.1021/acs.jafc.8b05829