RT Journal Article
SR Electronic
T1 Chondroitin Sulfate Elicits Systemic Pathogenesis In Mice By Interfering With Gut Microbiota Homeostasis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 142588
DO 10.1101/142588
A1 Liao, Tao
A1 Chen, Yan-Ping
A1 Huang, Shui-Qing
A1 Tan, Li-Li
A1 Li, Chang-Qing
A1 Huang, Xin-An
A1 Xu, Qin
A1 Wang, Qi
A1 Zeng, Qing-Ping
YR 2017
UL http://biorxiv.org/content/early/2017/05/27/142588.abstract
AB Whether chondroitin sulfate (CS), a common ingredient naturally occurring in livestock and poultry products, improves osteoarthritis remains debating. Here, we show for the first time that CS induces steatogenesis, atherogenesis, and dementia-like pathogenesis in mice. Gut microbiome analysis revealed the sulfatase-secreting bacteria Rikenella and the sulfate-reducing bacteria Desulfovibrio are enriched. Surprisingly, berberine use boosts CS-induced multi-loci inflammatory manifestations by further increasing the abundance of Rikenella and Desulfovibrio, whereas cephalosporin reinforces the colon mucus barrier via flourishing Akkermansia muciniphila and upregulating mucin expression. Mechanistically, berberine aggravates mucus lining injury by prompting mucin degradation, endotoxin leakage, neutralizing antibody induction, pro-inflammatory cytokine burst, lactic acid accumulation and energy currency depletion in multiple organs and tissues. Taken together, CS evokes the early-phase pathogenesis toward steatohepatitis, atherosclerosis, and dementia upon augmenting gut opportunistic infection, and a sustained antibiotic monotherapy does not deprive the risk of CS-driven systemic inflammatory disorders.