PT  - JOURNAL ARTICLE
AU  - Tao Liao
AU  - Yan-Ping Chen
AU  - Shui-Qing Huang
AU  - Li-Li Tan
AU  - Chang-Qing Li
AU  - Xin-An Huang
AU  - Qin Xu
AU  - Qi Wang
AU  - Qing-Ping Zeng
TI  - Chondroitin Sulfate Elicits Systemic Pathogenesis In Mice By Interfering With Gut Microbiota Homeostasis
AID  - 10.1101/142588
DP  - 2017 Jan 01
TA  - bioRxiv
PG  - 142588
4099  - http://biorxiv.org/content/early/2017/05/27/142588.short
4100  - http://biorxiv.org/content/early/2017/05/27/142588.full
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.