Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Du, Yong; Wu, Tianfu; Zhou, Xin J.; Davis, Laurie S.; Mohan, Chandra

doi:10.1007/s10753-016-0351-1

Cited by 12 publications

(9 citation statements)

References 32 publications

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“…Lo TH et al found that in the ureteral obstruction mouse model, TREM-1 regulated the polarization of macrophages [6]. Du et al further indicated that TREM-1 has the therapeutic value in anti-GBM-induced nephritis [16]. The polarization of macrophages played a vital role in renal fibrosis [17].…”

Section: Discussionmentioning

confidence: 99%

The ratio of urinary TREM-1/TREM-2 mRNA expression in chronic kidney disease and renal fibrosis

Cao

Wang²,

Peng³

et al. 2021

Annals of Medicine

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Background: The non-invasive identification of novel renal fibrosis biomarkers needs to be further studied. Methods: We collected urine samples from 77 biopsy-proven CKD patients and 15 healthy controls. The expression of urinary TREM-1 and TREM-2 was measured and the correlation with renal function parameter and pathological indicators was performed. The receiver operating characteristic (ROC) curve for the diagnosis of renal fibrosis was calculated. The protein expression of TREM-1 and TREM-2 in kidney tissues was measured. Results: The TREM-1/TREM-2 ratio was decreased in CKD patients and correlated with serum creatinine, estimated glomerular filtration rate and cystatin c. Further, the TREM-1/TREM-2 ratio was significantly decreased in moderate-severe fibrosis patients compared with none-mild renal fibrosis. TREM-1/TREM-2 ratio was correlated with the score of tubulointerstitial fibrosis (TIF) and the score of glomerular sclerosis. The ROC curve showed that the urinary TREM-1/TREM-2 ratio can diagnosemoderate-severe renal fibrosis at a cut-off value of 1.338 with a sensitivity of 86.4% and specificity of 81.8%. In human moderate-severe fibrosis kidney tissue, the protein expression of TREM-1 was lower and the TREM-2 was higher than none-mild fibrosis kidney tissue. Conclusion: Urinary TREM-1/TREM-2 ratio was a potential biomarker for the diagnosis of renal fibrosis in CKD patients.

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Section: Discussionmentioning

confidence: 99%

The ratio of urinary TREM-1/TREM-2 mRNA expression in chronic kidney disease and renal fibrosis

Cao

Wang²,

Peng³

et al. 2021

Annals of Medicine

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show abstract

“…In addition, TREM-1 is readily detected in biological fluids of patients suffering from a variety of disease 11 . 19 .…”

Section: Discussionmentioning

confidence: 99%

“…TREM-1 can be expressed by the inflammatory infiltrate and renal epithelial cells in chronic disease 19 .…”

Section: Discussionmentioning

confidence: 99%

Triggering Receptor Expressed on Myeloid Cells-1 and Clinical Disease Activity in Patient with SLE Nephritis 24 Months Follow-Up Study

Abdulhakim¹

2017

jmscr

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“…However, because of the limited quantity of IgA1-containing immune complexes isolated from circulation, we did not have enough IgA1-containing immune complexes for further experiments. Secondly, it was reported that urinary sTREM-1 levels are higher in patients with other kidney diseases, such as anti-GBM disease and acute kidney injury [24,28]; thus, it could not be a specific biomarker for IgAN. More studies are needed to evaluate its potential clinical implications in these kidney diseases.…”

Section: Elevated Urinary Strem-1 Levels In Patients With Iganmentioning

confidence: 99%

TREM-1 Contributes to Inflammation in IgA Nephropathy

Zhao¹,

Zhu²,

Liu³

et al. 2018

Kidney Dis

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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.

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Blockade of CD354 (TREM-1) Ameliorates Anti-GBM-Induced Nephritis

Cited by 12 publications

References 32 publications

The ratio of urinary TREM-1/TREM-2 mRNA expression in chronic kidney disease and renal fibrosis

The ratio of urinary TREM-1/TREM-2 mRNA expression in chronic kidney disease and renal fibrosis

Triggering Receptor Expressed on Myeloid Cells-1 and Clinical Disease Activity in Patient with SLE Nephritis 24 Months Follow-Up Study

TREM-1 Contributes to Inflammation in IgA Nephropathy

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