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Effect of tonsillar mononuclear cell supernatants in patients with IgA nephropathy on renal tubular epithelial cells

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Abstract

Objective

This study aimed to investigate the immunological relationship and the mechanism between tonsillar inflammation and immunoglobulin A nephropathy (IgAN).

Subjects

Tonsillar mononuclear cells (TMCs) were prepared from 13 patients with IgAN and 13 patients with chronic tonsillitis but without renal disease. The human renal tubular epithelial cell (TEC) line, HK-2, was used to test the effects of secretions from the TMCs.

Methods

Phytohemagglutinin (PHA) was used to induce the inflammatory responses in TMCs. The secretions from TMCs, stimulated with or without PHA, were collected and applied to HK-2 cells. The proliferation, apoptosis, and epithelial–mesenchymal transition (EMT) of HK-2 cells were evaluated. The expression of key components during apoptosis and EMT was measured.

Results

The secretions from PHA-stimulated IgAN TMCs significantly inhibited proliferation, promoted apoptosis, and down-regulated Bcl-2 in HK-2 cells (P < 0.05) in time- and concentration-dependent manners. They also modulated the expression of key components during EMT, E-cadherin and α-SMA (P < 0.05).

Conclusions

The secretions from PHA-stimulated IgAN TMCs can cause the inhibition of proliferation, promotion of apoptosis, down-regulation of Bcl-2, and EMT effects in HK-2 TECs, which may reflect the in-vivo remote modulation of functions of renal TECs by tonsillar inflammation.

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Acknowledgments

We thank Dr. Shousong Cao and Dr. Meir Wetzler of Roswell Park Cancer Institute (Buffalo, NY, USA) for proofreading the manuscript and for their invaluable suggestions.

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Correspondence to Youming Peng.

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Responsible Editor: Graham Wallace.

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Tang, Y., Peng, Y., Yang, S. et al. Effect of tonsillar mononuclear cell supernatants in patients with IgA nephropathy on renal tubular epithelial cells. Inflamm. Res. 62, 45–52 (2013). https://doi.org/10.1007/s00011-012-0549-0

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  • DOI: https://doi.org/10.1007/s00011-012-0549-0

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