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<p>The kidney-yang deficiency syndrome diarrhea (KDSD) is related to gut microbiota dysbiosis. The mechanism of the gut-kidney axis participating in regulating water metabolism in diarrhea remains to be studied. 30 male KM mice with SPF grade were randomly allocated into three groups: normal (NC), kidney-yang deficiency diarrhea (MD), and kidney-yang deficiency diarrhea aggravated by microbiota dysbiosis (MDA). Post-modeling assessments included kidney function, ADH, IL-6 and TNF-α levels. HE staining examined kidney and colon pathology. Immunohistochemistry assessed colonic mucosal barrier damage and AQP4 expression in colon and kidney tissues. 16S rRNA sequencing characterized gut microbial composition and diversity, supplemented by correlation analysis and metabolic function prediction. The model Mice exhibited an increase in fecal water content, and both colon and kidney tissues presented inflammatory infiltration and tissue damage. Additionally, serum Cr and BUN levels were elevated, IL-6 and TNF-α levels were increased, and ADH levels were reduced. The expression of AQP4, as well as the expression of ZO-1 and Occludin, decreased significantly. The microbiota in the colonic contents mainly manifested as a decline in richness, diversity, and evenness. Finally, <i>Phocaeicola_A</i> was significantly positively correlated with the expression of IL-6 and TNF-α, and significantly negatively correlated with the expression of ADH; <i>Bacteroides_H</i> was significantly negatively correlated with the expression of ADH and AQP4, and significantly positively correlated with inflammation factors. Gut microbiota dysbiosis compromises colonic mucosal integrity, elevates inflammatory markers in the kidney and colonic tissues, and induces pathological changes. This suppresses ADH and AQP4 expression, disrupting water metabolism via the gut-kidney axis. This constitutes the primary pathogenesis of KDSD.</p>

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Novel insights into diarrhea mechanism from gut-kidney axis perspective: correlations among intestinal mucosal injury, AQP4 water transport disorder and gut microbiota dysbiosis

  • 期刊论文

  • 发表日期：

    2026年3月25日

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  • Huiyi Peng,
  • Xinxin Peng,
  • Qin Liu,
  • Na Deng,
  • Xuejiao Xie,
  • Zhoujin Tan

摘要

The kidney-yang deficiency syndrome diarrhea (KDSD) is related to gut microbiota dysbiosis. The mechanism of the gut-kidney axis participating in regulating water metabolism in diarrhea remains to be studied. 30 male KM mice with SPF grade were randomly allocated into three groups: normal (NC), kidney-yang deficiency diarrhea (MD), and kidney-yang deficiency diarrhea aggravated by microbiota dysbiosis (MDA). Post-modeling assessments included kidney function, ADH, IL-6 and TNF-α levels. HE staining examined kidney and colon pathology. Immunohistochemistry assessed colonic mucosal barrier damage and AQP4 expression in colon and kidney tissues. 16S rRNA sequencing characterized gut microbial composition and diversity, supplemented by correlation analysis and metabolic function prediction. The model Mice exhibited an increase in fecal water content, and both colon and kidney tissues presented inflammatory infiltration and tissue damage. Additionally, serum Cr and BUN levels were elevated, IL-6 and TNF-α levels were increased, and ADH levels were reduced. The expression of AQP4, as well as the expression of ZO-1 and Occludin, decreased significantly. The microbiota in the colonic contents mainly manifested as a decline in richness, diversity, and evenness. Finally, Phocaeicola_A was significantly positively correlated with the expression of IL-6 and TNF-α, and significantly negatively correlated with the expression of ADH; Bacteroides_H was significantly negatively correlated with the expression of ADH and AQP4, and significantly positively correlated with inflammation factors. Gut microbiota dysbiosis compromises colonic mucosal integrity, elevates inflammatory markers in the kidney and colonic tissues, and induces pathological changes. This suppresses ADH and AQP4 expression, disrupting water metabolism via the gut-kidney axis. This constitutes the primary pathogenesis of KDSD.