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Published on: June 23, 2015
CD14 : a candidate biomarker for the prognosis of polycystic kidney disease
1Department of Anatomy and Cell Biology and the Kidney Institute, University of Kansas Medical Center, Kansas City, Kansas 66160, USA. gvandenheuvel@kumc.edu
Insights
CD14 expression indicates disease progression in polycystic kidney disease (PKD). This immune marker is found in renal tubule cells, suggesting early Toll-like receptor-4 activation in PKD.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Polycystic kidney disease (PKD) is a genetic disorder characterized by cyst formation in the kidneys.
- The role of the innate immune system in PKD pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the expression of innate immune markers in different models of PKD.
- To determine the correlation between CD14 expression and PKD progression.
- To explore the cellular origin of CD14 in the kidney and its implications for PKD.
Main Methods:
- Analysis of CD14 expression in the cpk mouse model of PKD.
- Examination of CD14 expression in human recessive and autosomal dominant PKD samples.
- Correlation analysis between CD14 levels and disease severity.
- Immunohistochemical analysis to identify CD14-expressing cells in the kidney.
Main Results:
- CD14 expression is validated in the innate immune system of PKD models and human patients.
- CD14 expression levels correlate with the progression of PKD, including early stages.
- CD14 is expressed by renal tubule epithelial cells, not solely inflammatory cells.
Conclusions:
- CD14 is a potential biomarker for PKD progression.
- Renal tubule epithelial cell expression of CD14 suggests an intrinsic mechanism of Toll-like receptor-4 activation in PKD.
- This activation may precede inflammatory cell infiltration in PKD pathogenesis.
Abstract:
Zhou et al. validate the expression of markers of the innate immune system in the cpk mouse model of polycystic kidney disease (PKD), in human recessive PKD, and in human autosomal dominant PKD and show that CD14 expression correlates with PKD progression, even from very early stages of disease. Moreover, they show that CD14 is expressed from the renal tubule epithelial cells, suggesting a mechanism of Toll-like receptor-4 activation in PKD prior to the infiltration of inflammatory cells.
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