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2017 ; 49
(8
): e370
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Enteric dysbiosis-linked gut barrier disruption triggers early renal injury
induced by chronic high salt feeding in mice
#MMPMID28857085
Hu J
; Luo H
; Wang J
; Tang W
; Lu J
; Wu S
; Xiong Z
; Yang G
; Chen Z
; Lan T
; Zhou H
; Nie J
; Jiang Y
; Chen P
Exp Mol Med
2017[Aug]; 49
(8
): e370
PMID28857085
show ga
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.