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Kidney Dis (Basel). 2018 Feb;4(1):29-36. doi: 10.1159/000485622. Epub 2018 Jan 12.

TREM-1 Contributes to Inflammation in IgA Nephropathy.

Zhao YF1,2,3,4, Zhu L1,2,3,4, Liu LJ1,2,3,4, Shi SF1,2,3,4, Lv JC1,2,3,4, Zhang H1,2,3,4.

Author information

1
Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China.
2
Peking University Institute of Nephrology, Beijing, China.
3
Key Laboratory of Renal Disease, Ministry of Health of China, Beijing, China.
4
Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing, China.

Abstract

Background:

Circulating IgA1-containing immune complexes (cIgA1) were shown to play important roles in IgA nephropathy (IgAN). They could induce the release of multiple inflammatory factors, including MCP-1 and IL-6, and elevated urinary inflammatory factors were also reported in patients with IgAN, which suggested that inflammation is a major contributor to kidney injury in IgAN. After the previous identification of the upregulated release of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) by mesangial cells under cIgA1 challenge using cytokine array, in the present study, we further explored the role of TREM-1, an amplifier of inflammation, in cIgA1-induced kidney injury.

Methods:

In total, 35 patients with IgAN and 17 healthy controls were enrolled. The cIgA1 was isolated from plasma and used to treat cultured mesangial cells. The mRNA expression of TREM-1 as well as levels of sTREM-1, MCP-1, and IL-6 in the mesangial cell supernatant and urine samples were detected.

Results:

We found that cIgA1 from patients with IgAN could significantly upregulate the expression of TREM-1 in mesangial cells compared to healthy controls. The levels of ΔsTREM-1 were positively correlated with MCP-1 levels in the mesangial supernatant. Similarly, higher urinary levels of sTREM-1 were also observed in patients with IgAN compared to healthy controls. Moreover, IgAN patients with detectable urinary sTREM-1 presented with severe clinical and pathological manifestations, including higher IgA and lower eGFR levels, compared to patients whose urinary sTREM-1 levels were below the limit of quantification.

Conclusion:

Our present study suggested that TREM-1 in cIgA1 induced inflammatory kidney injury in IgAN.

KEYWORDS:

Circulating IgA1-containing immune complexes; IgA nephropathy; TREM-1

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