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KMID : 0620920170490080009
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Experimental & Molecular Medicine
2017 Volume.49 No. 8 p.9 ~ p.9
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Enteric dysbiosis-linked gut barrier disruption triggers early renal injury induced by chronic high salt feeding in mice
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Hu Jing Juan
Luo Hai Hua
Wang Jie Yan
Tang Wen Li
Lu Jun Qi
Wu Shan
Xiong Zhi
Yang Gui Zhi
Chen Zhen Guo
Lan Tian
Zhou Hong Wei
Nie Jing
Jiang Yong
Chen Peng
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Abstract
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Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
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KEYWORD
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Experimental models of disease, Translational research
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